Abstract
Background:
Results from different studies on the effects of purslane consumption on blood pressure (BP) are still debated. To fill this knowledge gap, we investigated the overall effects of purslane consumption on systolic BP (SBP) and diastolic BP (DBP).
Materials and Methods:
A comprehensive literature search was conducted on Scopus, Web of Science, PubMed, Google Scholar, and Cochrane databases. A random-effect model was used to estimate the weighted mean difference (WMD) and 95% confidence interval (CI) for each outcome. Between studies heterogeneity was assessed by the I2 test. Prespecified subgroup analyses were performed to examine heterogeneity across sample size, age, sex, dosage, duration, and health status. This meta-analysis included randomized controlled trials (RCTs) involving adults (≥18 years) with either parallel or crossover designs. Studies must have included a control group, with the only intervention being purslane consumption and reported data suitable for calculating BP outcomes. Study quality was assessed using the Cochrane risk of Bias Tool and evidence certainty was rated through the grading of recommendations, assessment, development, and evaluation (GRADE) approach.
Results:
Five trials were included in the meta-analysis. Pooled analysis showed that purslane consumption significantly reduced SBP (WMD: −3.06 mmHg, 95% CI: −6.02 to − 0.11, P = 0.042; I2 = 95.5%, P < 0.001). However, purslane consumption did not change DBP (WMD: −0.62 mmHg, 95% CI: −2.01–0.87 P = 0.386; I2 = 81.7%, P < 0.001). Nevertheless, after subgroup analysis a significant decrease in DBP levels was observed among participants who were older than 40 years, had diabetes, and underwent a 12-week intervention. According to the GRADE assessment, the certainty of evidence for SBP was rated as moderate due to serious concerns about indirectness, whereas the evidence for DBP was rated as low quality because of significant limitations related to both imprecision and indirectness.
Conclusion:
Our findings suggest that purslane consumption may have a modest but clinically significant effect on reducing SBP compared to placebo and may improve DBP in specific subgroups. Given that even small reductions in SBP are associated with important reductions in cardiovascular risk, purslane may represent a promising complementary nutritional strategy for BP management. However, further well-designed RCTs with larger sample sizes are needed to confirm these effects and assess their long-term clinical significance.
Keywords: Blood pressure, meta-analysis, purslane, systematic review
INTRODUCTION
High blood pressure (BP) is the key preventable risk factor for all-cause mortality, especially cardiovascular disease.[1] It was the cause of death for 10.8 million people in 2019 alone; over the last half-century, due to factors such as population aging, sedentary lifestyle, obesity, and improper diet, the number of people with high BP has increased significantly (90%).[2] Hypertension is confirmed when a high systolic BP (SBP) (≥135 mmHg) or diastolic BP (DBP) (≥85 mmHg) is measured at more than one visit.[3] Despite the widespread use of first-line antihypertensive medications such as long-acting calcium channel blockers, diuretics, angiotensin-converting enzyme inhibitors, beta-blockers, and angiotensin II receptor blockers, BP control remains suboptimal, with fewer than half of patients achieving target levels. This persistent gap has spurred growing interest in alternative therapies, including medicinal plants, which have been traditionally valued for their beneficial properties. Given challenges such as side effects, poor medication adherence, and high costs, plant-based interventions–particularly those rich in bioactive compounds–are increasingly being examined for their potential role in managing elevated BP.[4,5]
Portulaca oleracea (purslane) is one such herbal medicine that is commonly found on all continents. This plant is described in Chinese folklore as a “vegetable for long life.”[6] Purslane is a nutrient-rich medicinal plant recognized for its broad spectrum of therapeutic properties, including anti-inflammatory, antioxidant, antihypertensive, antidiabetic, hepatoprotective, neuroprotective, and wound-healing effects. It contains an abundance of essential Vitamins (A, B, C, and E), key minerals (magnesium, zinc, calcium, and phosphorus), and beneficial phytochemicals such as alkaloids, flavonoids, and terpenoids.[7,8] Purslane is also among the richest botanical sources of omega-3 fatty acids particularly α-linolenic acid, gamma-linolenic acid, and linoleic acid which have been revealed to support vascular function through vasodilatory (enhance endothelial nitric oxide synthase activity) and anti-inflammatory (suppress proinflammatory cytokines) mechanisms.[9] Its elevated levels of magnesium and potassium further promote electrolyte balance and endothelial health, while antioxidants and flavonoids such as Vitamins E, C, and β-carotene help decrease oxidative stress, a central factor in the development of hypertension.[10] Taken together, these synergistic components highlight purslane’s exceptional potential as a natural agent for BP regulation, distinguishing it from other medicinal herbs.
Chronic hypertension has a lot of complications, for example, it increases some mediators such as the reactive oxygen species (ROS), proinflammation molecules, and endothelin-1 (the most potent vasoconstrictor) and as a result, matrix metalloproteinases (MMPs) are activated.[11] Hence, any agent like purslane as an herbal medicine that inhibit the activation of MMPs can be effective in reducing high BP.[6,12] The results of studies in populations with the lowest mortality rate from heart diseases showed that these people follow a diet containing sufficient amounts of eicosapentaenoic acid from fresh fish as well as linolenic acid found in purslane and walnuts.[13] A human study showed that the consumption of 60 mg purslane extract significantly reduces SBP without causing severe side effects.[14] An animal study revealed that the ethanol extract of purslane was able to inhibit the increase in BP compared to the control group.[15] The results of another animal indicated that feeding purslane (300 mg/kg/day) for 10 weeks improved lipid profiles, decreased SBP level, endothelin-1, and MMPs significantly.[16]
While several individual trials have investigated purslane’s effects on BP, no prior study has systematically synthesized this evidence using robust frameworks for evidence certainty and clinical relevance. Given the growing body of evidence regarding the metabolic and vascular benefits of purslane, this systematic review and meta-analysis of randomized controlled trials (RCTs) was conducted to quantitatively assess its effects on SBP and DBP. To enhance and extend existing research, we applied the grading of recommendations, assessment, development, and evaluation (GRADE) framework to evaluate the certainty of evidence, performed subgroup analyses to investigate potential effect modifiers (e.g., participant health status dosage, and intervention duration), and examined clinical applicability across varied trial contexts. This methodology offers a more rigorous and comprehensive synthesis compared to previous narrative or descriptive reviews.
METHODS
The procedures of the current study were followed by the Preferred Reporting Items for Systematic Review and Meta-Analysis [Supplementary Table 1].[17] This meta-analysis was recorded in PROSPERO with the code CRD42023428940.
Supplementary Table 1.
Preferred reporting items for systematic review and meta-analysis checklist
| Section/topic | Number | Checklist item | Reported on page number | |
|---|---|---|---|---|
|
Title
| ||||
| Title | 1 | Identify the report as a systematic review, meta-analysis, or both | Page 1 | |
|
Abstract | ||||
| Structured summary | 2 | Provide a structured summary including, as applicable: Background; objectives; data sources; study eligibility criteria, participants, and interventions; study appraisal and synthesis methods; results; limitations; conclusions and implications of key findings; systematic review registration number | Page 2 | |
|
Introduction | ||||
| Rationale | 3 | Describe the rationale for the review in the context of what is already known | Page 3 | |
| Objectives | 4 | Provide an explicit statement of questions being addressed with reference to PICOS | Page 4 | |
|
Methods | ||||
| Protocol and registration | 5 | Indicate if a review protocol exists, if and where it can be accessed (e.g., Web address), and, if available, provide registration information including registration number | Page 4 | |
| Eligibility criteria | 6 | Specify study characteristics (e.g., PICOS, length of follow-up) and report characteristics (e.g., years considered, language, publication status) used as criteria for eligibility, giving rationale | Page 5 | |
| Information sources | 7 | Describe all information sources (e.g., databases with dates of coverage, contact with study authors to identify additional studies) in the search and date last searched | Page 4 | |
| Search | 8 | Present full electronic search strategy for at least one database, including any limits used, such that it could be repeated | Page 4 | |
| Study selection | 9 | State the process for selecting studies (i.e., screening, eligibility, included in systematic review, and, if applicable, included in the meta-analysis) | Page 5 | |
| Data collection process | 10 | Describe method of data extraction from reports (e.g., piloted forms, independently, in duplicate) and any processes for obtaining and confirming data from investigators | Page 5 Page 6 |
|
| Data items | 11 | List and define all variables for which data were sought (e.g., PICOS, funding sources) and any assumptions and simplifications made | Page 5 | |
| Risk of bias in individual studies | 12 | Describe methods used for assessing risk of bias of individual studies (including specification of whether this was done at the study or outcome level), and how this information is to be used in any data synthesis | Page 10 | |
| Summary measures | 13 | State the principal summary measures (e.g., risk ratio, difference in means) | Page | |
| Synthesis of results | 14 | Describe the methods of handling data and combining results of studies, if done, including measures of consistency (e.g., I2) for each meta-analysis | Page 6 | |
| Risk of bias across studies | 15 | Specify any assessment of risk of bias that may affect the cumulative evidence (e.g., publication bias, selective reporting within studies) | Page 10 | |
| Additional analyses | 16 | Describe methods of additional analyses (e.g., sensitivity or subgroup analyses, meta-regression), if done, indicating which were prespecified | Page 6 | |
|
Results | ||||
| Study selection | 17 | Give numbers of studies screened, assessed for eligibility, and included in the review, with reasons for exclusions at each stage, ideally with a flow diagram | Page 7 | |
| Study characteristics | 18 | For each study, present characteristics for which data were extracted (e.g., study size, PICOS, follow-up period) and provide the citations | Page 7, and Table 1 | |
| Risk of bias within studies | 19 | Present data on risk of bias of each study and, if available, any outcome level assessment (see item 12) | Figures 2 | |
| Results of individual studies | 20 | For all outcomes considered (benefits or harms), present, for each study: (a) simple summary data for each intervention group (b) effect estimates and confidence intervals, ideally with a forest plot | [Figures 3–4] | |
| Synthesis of results | 21 | Present results of each meta-analysis done, including confidence intervals and measures of consistency | [Figures 3–4] | |
| Risk of bias across studies | 22 | Present results of any assessment of risk of bias across studies (see Item 15) | [Figures 2] | |
| Additional analysis | 23 | Give results of additional analyses, if done (e.g., sensitivity or subgroup analyses, meta-regression, see item 16) | Supplementary Tables 1 | |
|
Discussion | ||||
| Summary of evidence | 24 | Summarize the main findings including the strength of evidence for each main outcome; consider their relevance to key groups (e.g., healthcare providers, users, and policy makers) | Page 10 | |
| Limitations | 25 | Discuss limitations at study and outcome level (e.g., risk of bias), and at review-level (e.g., incomplete retrieval of identified research, reporting bias) | Page 12 | |
| Conclusions | 26 | Provide a general interpretation of the results in the context of other evidence, and implications for future research | Page 12 | |
|
Funding | ||||
| Funding | 27 | Describe sources of funding for the systematic review and other support (e.g., supply of data); role of funders for the systematic review | Page 12 | |
PICOS=Participants, interventions, comparisons, outcomes, and study design
Search strategy
The following electronic databases were used to find pertinent RCTs up to April 2025: ISI Web of Science, PubMed, Cochrane databases, and Scopus. The subject headings (MeSH) and non-MeSH keywords (Portulaca, OR Portulaca oleracea OR Purslane AND Hypertension OR BP OR Blood pressure OR Diastolic blood pressure OR Systolic blood pressure OR SBP OR DBP OR Metabolic syndrome OR MetS) were used. The searches conducted on various databases had no limitations regarding language or date. Furthermore, references from related review papers and selected studies were screened manually to identify any studies that might have been missed.
Inclusion and exclusion criteria
The present meta-analysis included RCTs that fulfilled the following criteria: (I) the studies designed as RCTs with parallel or crossover designs, (I) the study participants were adults aged 18 years and above, (III) the studies had to have a control group and the only difference between the studied groups was the purslane consumption, and (IV) the RCTs needed to report mean ± standard deviation (SD) or other data to calculate these values for the effects of purslane on BP (primary or secondary outcome). Studies that were conducted on animals, children (<18), pregnant and lactating women, as well as observational and review articles were excluded from the study.
Data extraction
Two authors (M.V. and Sh.H.) independently extracted data from each eligible RCT, including the first author’s name, country of origin, publication year, group-specific sample sizes, duration of intervention, purslane dosage, and key participant characteristics (mean age, gender, and health status). BP values–expressed as mean ± SD at baseline, postintervention, and as change scores–were also collected. Any discrepancies between reviewers were resolved through discussion with a third author (G.A.). For studies with missing or unreported data, we attempted to contact the corresponding authors to obtain the necessary information. If no response was received, we followed imputation strategies recommended by the Cochrane Handbook, deriving missing means or SDs from alternative reported statistics such as confidence intervals (CIs) or interquartile ranges to maintain consistency and minimize bias across the analysis.
Quality assessment
Two investigators (M.V. and Sh.H.) used the Cochrane risk of bias tool for RCTs[18] to identify the quality of included articles. This tool consists of several components, including (I) sufficient random sequence generation, (II) allocation concealment, (III) blinding of staff and entire procedures, (IV) indicates incomplete data, (V) selected outcome report, and (VI) other possible sources of bias. The Cochrane Handbook recommends classifying RCTs into three categories based on bias: low risk, moderate risk, and high risk. In case of any disagreements during the quality assessment, a third reviewer (G.A.) would have been consulted.
Certainty assessment
The quality of evidence was assessed using the GRADE protocol. In accordance with this approach, the assessment was based on factors such as risk of bias, indirectness, inconsistency, publication bias, and imprecision. Based on the assessment criteria, the quality of the evidence was categorized as either very low, low, moderate, or high.[19]
Data synthesis and statistical analysis
The meta-analysis was accomplished by fulfilling STATA statistical software (version 14; StataCorp, College Station, Lakeway, TX, USA). We inserted the mean change and SD change of DBP and SBP levels and used them to calculate the pooled effects. In case the results were not reported as means ± SD in an RCT, they were converted with appropriate statistical formulas.[20] Furthermore, if mean changes were not reported, we computed them by using the formula: mean change = final BP values – baseline BP values. Similarly, SD changes were calculated using the formula: SD change = square root ([SD baseline] 2+ [SD final] 2 – [2R × SD baseline × SD final]), R = (SD12 + SD22 – SDchange2)/(2 × SD1 × SD2).[21] Treatment effects were determined as weighted mean differences (WMDs) and 95% CIs, and we used random effect models to estimate the overall effect size.[22] To assess the variation between studies, we used the I-square (I2) index. It is noteworthy that if I2 is above 50%, it indicates a significant heterogeneity between the studies.[23] Furthermore, to check potential sources of heterogeneity, subgroup analyses were conducted following the preplanned criteria, including sample size (<60 vs. ≥60), purslane dose (<10,000 mg vs. 10,000 mg), duration of intervention (8 weeks vs. 12 weeks), sex (female vs. Both), age (<40 vs. ≥40 years), and health status (diabetes, NAFLD, metabolic syndrome [MetS]/obesity). Meta-regression analysis using the random-effects model was undertaken to examine the potential association between variations in dose and duration with BP. During our analysis, we utilized visual inspection of funnel plot tests and Egger’s linear regression test to effectively assess publication bias.[24,25] In addition, a sensitivity analysis was carried out to evaluate how each trial influenced the overall effect size. Statistical significance was determined by considering P < 0.05 in all analyses.
RESULTS
Study selection
A total of 684 papers were identified through our initial literature search. After removing 128 duplicates, 554 studies remained for screening. According to predefined inclusion and exclusion criteria, 523 studies were excluded after screening the titles and abstracts. Therefore, 31 relevant studies remained for full-text review. Among these, 26 studies were excluded because of a lack of required data reporting. Finally, five trials achieving all needed criteria were included for meta-analysis in the current study [Figure 1].
Figure 1.

Flow diagram of study screening and selection process
Study characteristics
Study characteristics of the five studies[14,26,27,28,29] are shown in Table 1. In total, 300 participants were included (case = 152 and control = 148) in these publications dated between 2016 and 2021. The mean age of the participants ranged between 40 and 52 years. Study durations ranged from 8 to 12 weeks with sample sizes ranging from 48 to 71 participants. While the majority of trials enrolled both sexes, one study exclusively utilized female participants.[29] These studies were conducted in Iran[26,27,28,29] and Israel.[14] Two studies included patients with NAFLD;[26,28] two studies were performed in patients with type 2 diabetes mellitus (T2DM);[14,27] and one study enrolled participants with MetS.[29]
Table 1.
Characteristics of included studies in the systematic review and meta-analysis
| First author | Year/Country | Study design | Subject | Participants (intervention/control) | Mean age (intervention/control) | Baseline BMI (intervention/control) | Duration (week) | Type of administration |
Main results | |
|---|---|---|---|---|---|---|---|---|---|---|
| Intervention | Placebo | |||||||||
| Darvish Damavandi et al. | 2020 Iran | Randomized, double-blind clinical trial | NAFLD | 37/37 | 46.18/46.05 | 31.56/31.83 | 12 | 300 mg purslane extract | Placebo | There are no significant changes in BP |
| Papoli et al. | 2019 Iran | Randomized clinical trial | MetS | 32/32 | 42.16/43.16 | 28.23/26.30 | 12 | 10 g purslane seed +150 cc low-fat yogurt | 150 cc low-fat yogurt | Significant reductions in weight, and WC. There are no significant changes in BP |
| Gheflati et al. | 2019 Iran | Randomized controlled clinical trial | NAFLD | 27/27 | 40.07/39.81 | 32.77/31.08 | 8 | 10 g of purslane seeds + weight loss diet | Weight loss diet | There are no significant changes in BP |
| Wainstein et al. | 2016 Israel | Double-blind, placebo-controlled clinical trial | Type 2 diabetes | 31/32 | 52.4/58.3 | 29.9/29.1 | 12 | 180 mg/day Portusana | Placebo | SBP was reduced significantly more in the purslane group than in the placebo group |
| Esmaillzadeh et al. | 2015 Iran | Randomized controlled cross-over clinical trial | Type 2 diabetes | 48 | 51.4 | 28.99 | 12 | 10 g/day purslane seeds +240 cc low-fat yogurt | 240 cc low-fat yogurt | Significant reduction in weight and BMI, SBP, and DBP |
BMI=Body mass index; WC=Waist circumference; BP=Blood pressure; DBP=Diastolic BP; SBP=Systolic BP; NAFLD=Nonalcoholic fatty liver disease; MetS=Metabolic syndrome
Risk of bias assessment, and grading of recommendations, assessment, development, and evaluation assessment
The results of the risk of bias assessment for the included trials are presented in Figure 2. All studies demonstrated a low risk of bias in domains related to allocation concealment, random sequence generation, and participant blinding. However, approximately 80% of trials showed a high risk of bias in the domain of selective reporting. In addition, 60% of studies were rated as having a high risk of bias due to issues with blinding of outcome assessment and incomplete outcome data. The GRADE profile for the certainty of the evidence is included in Supplementary Table 2. Based on the GRADE assessment, the overall certainty of evidence for SBP was rated as moderate, primarily due to serious concerns about indirectness including variability in study populations and intervention contexts that limited generalizability. In contrast, the evidence for DBP was rated as low quality, reflecting serious limitations in both imprecision, such as wide CIs and small sample sizes, and indirectness, due to discrepancies between study settings and the target population.
Figure 2.

Results of risk of bias assessment for trials included in the current meta-analysis on the effects of purslane supplementation on blood pressure
Supplementary Table 2.
Grading of recommendations, assessment, development, and evaluation approach summary of findings and quality of evidence assessment
| Outcome | Number of studies | Design | Risk of bias | Inconsistency | Indirectness | Imprecision | Publication bias | Quality of evidence |
|---|---|---|---|---|---|---|---|---|
| SBP | 5 | RCTs | Seriousa | No seriousb | Seriousc | No seriousd | No seriouse | Moderate |
| DBP | 5 | RCTs | Serious | No serious | Serious | Serious | No serious | Low |
aFor risk of bias; the majority of included studies were considered to be at high risk of bias; bDowngraded if there was a substantial unexplained heterogeneity (I2>50%, P<0.10) that was unexplained by meta-regression or subgroup analyses; cDowngraded if there were factors present relating to the participants, interventions, or outcomes that limited the generalizability of the results; dOptimal information size was not met, or the 95% CI include the null value lower and upper bounds of the 95% CI were <0.95 and >1.05, respectively; eDowngraded if there was an evidence of publication bias using funnel plot. The quality of evidence is divided into 4 levels using GRADE system (high, moderate, low, very low). DBP=Diastolic BP; SBP=Systolic BP; RCTs=Randomized controlled trials; GRADE=Grading of recommendations, assessment, development, and evaluation; CI=Confidence interval
Effect of purslane supplementation on systolic blood pressure
Pooled analysis of five RCTs suggested that purslane supplementation significantly decreased SBP levels (WMD: −3.06 mmHg, 95% CI: −6.02 to −0.11, P = 0.042). A significant heterogeneity was observed across studies (I2 = 95.5%, P < 0.001) [Figure 3]. Subgroup analysis was conducted to examine sources of heterogeneity. Subgroup analysis shows that health status explains the heterogeneity. After subgroup analysis, we observed that the effect of purslane supplementation on SBP was more robust at the dosages of < 10 g/d (WMD: −6.34 mmHg, 95% CI: −7.95 to −4.73, P < 0.001; I2 = 89.6%, P = 0.002), in trials that were treated for 12 weeks (WMD: −4.48 mmHg, 95% CI: −5.35 to −3.61, P < 0.001; I2 = 82.8%, P = 0.001) and in studies performed on subjects with diabetes (WMD: −4.85 mmHg, 95% CI: −5.78 to −3.92, P < 0.001; I2 = 91.6%, P = 0.001) [Supplementary Table 3].
Figure 3.

Forest plot illustrating weighted mean difference and 95% confidence intervals for the impact of purslane on systolic blood pressure
Supplementary Table 3.
Results of subgroup analyses for the effects of purslane supplementation on systolic blood pressure according to intervention or participant characteristics
| Study group | Number of effect sizes | WMD (95% CI) | P-effect | P heterogeneity | I2 (%)3 | P for between-subgroup heterogeneity |
|---|---|---|---|---|---|---|
| Sample size (n) | ||||||
| <60 | 2 | −0.79 (−1.22, −0.35) | 0.001 | <0.001 | 97.2 | 0.001 |
| ≥60 | 3 | −5.59 (−7.02, −4.15) | 0.001 | 0.001 | 85.5 | |
| Dose (mg) | ||||||
| <10,000 | 2 | −6.34 (−7.95, −4.73) | <0.001 | 0.002 | 89.6 | <0.001 |
| 10,000 | 3 | −0.82 (−1.25, −0.39) | <0.001 | <0.001 | 94.5 | |
| Duration (week) | ||||||
| 8 | 1 | −0.23 (−0.69, 0.23) | 0.337 | - | - | <0.001 |
| 12 | 4 | −4.48 (−5.35, −3.61) | <0.001 | 0.001 | 82.8 | |
| Sex | ||||||
| Female | 1 | −2.65 (−5.83, 0.53) | 0.102 | - | - | 0.364 |
| Both | 4 | −1.16 (−1.58, −0.74) | <0.001 | <0.001 | 96.6 | |
| Age (years) | ||||||
| <40 | 1 | −0.23 (−0.69, 0.23) | 0.337 | - | - | <0.001 |
| ≥40 | 4 | −4.48 (−5.35, −3.61) | <0.001 | 0.001 | 82.8 | |
| Health status | ||||||
| Diabetes | 2 | −4.85 (−5.78, −3.92) | <0.001 | 0.001 | 91.6 | <0.001 |
| NAFLD | 2 | −0.23 (−0.70, 0.23) | 0.321 | 0.828 | 0 | |
| MetS and obesity | 1 | −2.65 (−5.83, 0.53) | 0.102 | - | - | |
MetS=Metabolic syndrome; CI=Confidence interval; WMD=Weighted mean difference; NAFLD=Nonalcoholic fatty liver disease
Effect of purslane supplementation on diastolic blood pressure
Pooling five RCTs together did not indicate a significant effect of purslane supplementation on DBP (WMD: −0.62 mmHg, 95% CI: −2.01 to 0.87, P = 0.386) in comparison with the placebo group. A high heterogeneity was found among the RCTs (I2 = 81.7%, P < 0.001) [Figure 4]. Subgroup analysis showed that sample size, dose, health status, duration, and age explain the heterogeneity. After subgroup analysis, we observed that the effect of purslane supplementation on DBP was more robust in trials that treated for 12 weeks (WMD: −1.60 mmHg, 95% CI: (−2.37 to −0.84, P < 0.001; I2 = 46.6%, P = 0.132), in studies performed on subjects with diabetes (WMD: −2.01 mmHg, 95% CI: −2.84 to −1.17, P < 0.001; I2 = 0%, P = 0.746), and in studies on subjects with a mean age of ≥40 years old (WMD: −1.60 mmHg, 95% CI: −2.37 to −0.84, P < 0.001; I2 = 46.6%, P = 0.132) [Supplementary Table 4].
Figure 4.

Forest plot illustrating weighted mean difference and 95% confidence intervals for the impact of purslane on diastolic blood pressure. WMD: Weighted mean difference
Supplementary Table 4.
Results of subgroup analyses for the effects of purslane supplementation on diastolic blood pressure according to intervention or participant characteristics
| Study group | Number of effect sizes | WMD (95% CI) | P-effect | P- heterogeneity | I2 (%)3 | P for between-subgroup heterogeneity |
|---|---|---|---|---|---|---|
| Sample size (n) | ||||||
| <60 | 2 | −0.19 (−0.52, 0.13) | 0.251 | <0.001 | 95.2 | 0.879 |
| ≥60 | 3 | −0.06 (−1.68, 1.55) | 0.939 | 0.570 | 0 | |
| Dose (mg) | ||||||
| <10,000 | 2 | −0.78 (−3.11, 1.53) | 0.507 | 0.528 | 0 | 0.609 |
| 10,000 | 3 | −0.17 (−0.50, 0.15) | 0.290 | <0.001 | 90.5 | |
| Duration (week) | ||||||
| 8 | 1 | 0.12 (−0.23, 0.47) | 0.507 | - | - | <0.001 |
| 12 | 4 | −1.60 (−2.37,−0.84) | <0.001 | 0.132 | 46.6 | |
| Sex | ||||||
| Female | 1 | 0.61 (−1.63, 2.87) | 0.591 | - | - | 0.479 |
| Both | 4 | −0.20 (−0.52, 0.12) | 0.219 | <0.001 | 85.9 | |
| Age (years) | ||||||
| <40 | 1 | 0.12 (−0.23, 0.47) | 0.507 | - | - | <0.001 |
| ≥40 | 4 | −1.60 (−2.37, −0.84) | <0.001 | 0.132 | 46.6 | |
| Health status | ||||||
| Diabetes | 2 | −2.01 (−2.84, −1.17) | <0.001 | 0.746 | 0 | <0.001 |
| NAFLD | 2 | 0.11 (−0.23, 0.47) | 0.510 | 0.945 | 0 | |
| MetS and obesity | 1 | 0.61 (−1.63, 2.87) | 0.591 | - | - | |
MetS=Metabolic syndrome; CI=Confidence interval; WMD=Weighted mean difference; NAFLD=Nonalcoholic fatty liver disease
Meta-regression analysis
The results of the meta-regression test showed that there was no significant association between the dosage and duration of purslane supplementation and alterations in SBP, and DBP [Supplementary Figure 1 (1.2MB, tif) a-d].
Sensitivity analysis
Sensitivity analysis for DBP showed that the overall estimates were not influenced by the elimination of any study. Sensitivity analysis for SBP shows that the exclusion of Papoli et al. (WMD: −3.14 mmHg, 95% CI: −6.53–0.23),[29] Wainstein et al. (WMD: −1.89 mmHg, 95% CI: −4.40–0.61),[14] and Esmaillzadeh et al. (WMD: −2.81 mmHg, 95% CI: −7.07–1.44)[27] studies changes the overall effect size to be statistically nonsignificant [Supplementary Figure 2 (645.5KB, tif) a and b]. These studies may have exerted a disproportionate influence on the overall pooled estimate due to distinct methodological and clinical characteristics. For example, Esmaillzadeh et al.[27] implemented a crossover design with a short intervention period (5 weeks) and a small sample of individuals with T2DM, which may have produced condition-specific or unstable treatment effects. Papoli et al.[29] examined a homogeneous cohort of middle-aged women with MetS and applied a longer intervention duration (12 weeks), potentially amplifying treatment responsiveness. Wainstein et al.[14] investigated patients with T2DM receiving concurrent pharmacotherapy, introducing potential confounding related to baseline medication use and metabolic variability. Together, these design-specific and population-level differences likely contributed to heterogeneity across studies, highlighting the need to carefully consider individual trial contexts when interpreting synthesized outcomes.
Publication bias
Funnel plots showed evidence of moderate asymmetry in the effects of purslane supplementation on BP [Figure 5a and b]. In contrast, Egger’s regression tests provided no evidence of publication bias for SBP (P = 0.257) and DBP (P = 0.565). The discrepancy between Egger’s test and funnel plot asymmetry may be attributed to methodological heterogeneity and low statistical power, such as differences in population characteristics, intervention duration, and dosage which could have influenced effect estimates irrespective of reporting bias. According to Cochrane guidance, asymmetry in funnel plots with < 10 studies should be interpreted with caution.
Figure 5.

Funnel plot (with pseudo 95% confidence intervals) of the weighted mean difference (WMD) versus the se (WMD) for studies evaluating the association between purslane supplementation and systolic blood pressure (a), and diastolic blood pressure (b) values. WMD: Weighted mean difference
DISCUSSION
As far as we know, this was the first systematic review and meta-analysis of RCTs on the effect of purslane consumption and BP comprehensively. In this study, purslane consumption significantly improved SBP levels compared to control groups. However, the overall effect size of SBP is statistically nonsignificant after eliminating Papoli et al.,[29] Wainstein et al.,[14] and Esmaillzadeh et al.[27] studies. Participants in these studies had different baseline SBP levels, different dosages of purslane, different purslane types, and various health conditions that could influence the observed results. In addition, purslane consumption did not change substantially DBP levels. Nevertheless, a significant decrease in DBP levels was observed among participants who were older than 40 years, had diabetes, and underwent a 12-week intervention. Purslane may be more effective in diabetics because previous studies indicated that it is beneficial for managing glycemic indexes and has antidiabetic properties.[30] Since diabetes and BP are closely related, controlling blood sugar in diabetics may help control their BP.[31]
Research suggests that purslane consumption may positively influence BP regulation, particularly in individuals with T2DM.[27] A study found that a 60 mg dose of purslane significantly reduced SBP in the overall cohort[14] whereas another study by Darvish Damavandi et al.[26] reported that a 12-week supplementation of 300 mg/day had no significant impact on SBP or DBP. In addition, daily consumption of three g of purslane leaves with dinner was associated with improved lipid metabolism and reduced hypercholesterolemia, potentially lowering cardiovascular risk. While animal studies highlight the BP-lowering properties of ethanol extracts and long-term supplementation (300 mg/kg/day), which improved lipid profiles and SBP levels over 10 weeks.[15] Purslane seeds and extracts exhibit distinct biochemical profiles and absorption dynamics, shaping their therapeutic applications.[32] Seeds are rich in fiber, proteins, and essential omega-3 fatty acids, complemented by flavonoids and phenolic compounds.[33] However, their natural matrix requires enzymatic digestion, delaying nutrient release. Conversely, extracts undergo refinement to concentrate bioactive compounds such as alkaloids and polysaccharides, enhancing potency and bioavailability.[34] Extracts bypass digestion, entering circulation more swiftly and exerting faster therapeutic effects.[34] These disparities highlight the need to account for formulation differences when evaluating purslane’s clinical efficacy.
Furthermore, the positive effect of purslane consumption on BP may be attributed to its nutrient content, including flavonoids and alpha-lipoic acid (ALA).[32] The beneficial effects of flavonoids and ALA on BP have been indicated in some studies.[35,36,37,38] The use of ALA supplements can significantly reduce elevated SBP by inhibiting the reduction of sirtuin 3, hyperacetylation of superoxide dismutase 2, and the overproduction of ROS in mitochondria.[26] In line with our results, omega-3 fatty acids are more effective in reducing SPB than DBP.[39,40] Studies have indicated that omega-3 fatty acids lower BP by increasing endothelial nitric oxide and decreasing angiotensin-converting enzyme activity.[39,41] The suppression of the renin–angiotensin system may be related to peroxisome proliferator-activated receptor gamma (PPARy) activation.[14] Activation of PPARy inhibits adhesion cascades and harmful inflammatory events in the vascular system. So, hypertension can be treated by direct endothelial functional regulation and vascular anti-inflammatory mechanisms induced by PPARy activation in individuals.[42] Another mechanism for lowering BP is related to MMPs. MMPs change the smooth muscle tone, and it could create a vicious cycle of rising BP.[43,44] The results of an animal study indicated that purslane intake could decrease SBP levels, endothelin-1, and MMPs significantly.[16] So, any agent like purslane that inhibits the activation of MMPs can be effective in reducing high BP.[6,12] According to purslane’s positive effect on high BP, it may be recommended to include it in hypertension dietary management.
Side effects
The side effects of purslane have only been studied in a few studies. The presence of high levels of oxalate in purslane has been linked to hyperoxaluria, calcium oxalate crystals, and kidney stones.[45] Recent research demonstrated that consuming 0.75 kg of purslane in a single meal could cause nephropathy due to oxalate.[46] The absorption of soluble oxalate may be reduced by consuming purslane with yogurt.[45] Nonetheless, daily consumption of purslane is still questionable.
Strengths and limitations
This meta-analysis has several strengths: first, different confounders were used to conduct subgroup analyses, second, a thorough sensitivity analysis was conducted to ensure stable results, third, the GRADE method was used to determine the certainty of outcomes. Despite this, there are a few limitations to be considered. The included studies differed greatly based on the type of purslane consumed, the dosage, and the health status of participants. In addition, a small number of studies were included. Finally, the included studies were heterogeneous. To identify the heterogeneity sources, we conducted subgroup analyses based on a variety of variables.
CONCLUSION
The results of this meta-analysis demonstrated a significant reduction in SBP levels following purslane consumption, highlighting its potential role in clinical BP management. To enhance the understanding of its therapeutic effects, future clinical trials should investigate varying doses of purslane, considering its potential integration into evidence-based management practices. Moreover, further prospective studies with larger populations across diverse geographic regions and extended durations are necessary to determine the consistency and long-term effectiveness of purslane in lowering BP in clinical settings.
Ethical consideration
Ethics approval and registration were obtained from the Isfahan University of Medical Sciences ethical committee (IR.MUI.RESEARCH.REC.1402.159). The study protocol was registered in PROSPERO.
Data availability
Data will be made available on request.
Conflicts of interest
There are no conflicts of interest.
Random-effects meta-regression plots of the association between mean changes in systolic blood pressure (a and b), and diastolic blood pressure (c and d) and purslane dose and intervention duration
Sensitivity analysis of purslane on diastolic blood pressure (a), and systolic blood pressure (b)
Acknowledgments
We are grateful for the support of the Student Research Committee, Isfahan University of Medical Sciences (grant number: 1402108).
Funding Statement
Nil.
REFERENCES
- 1.Mills KT, Stefanescu A, He J. The global epidemiology of hypertension. Nat Rev Nephrol. 2020;16:223–37. doi: 10.1038/s41581-019-0244-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Schutte AE, Jafar TH, Poulter NR, Damasceno A, Khan NA, Nilsson PM, et al. Addressing global disparities in blood pressure control: Perspectives of the International Society of Hypertension. Cardiovasc Res. 2023;119:381–409. doi: 10.1093/cvr/cvac130. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Whelton PK. Epidemiology of hypertension. Lancet. 1994;344:101–6. doi: 10.1016/s0140-6736(94)91285-8. [DOI] [PubMed] [Google Scholar]
- 4.Mohammed SA, Hanxing L, Fang L, Algradi AM, Alradhi M, Safi M, et al. Integrated Chinese herbal medicine with Western Medicine versus Western Medicine in the effectiveness of primary hypertension treatment: A systematic review and meta-analysis of randomized controlled trials. J Ethnopharmacol. 2023;300:115703. doi: 10.1016/j.jep.2022.115703. [DOI] [PubMed] [Google Scholar]
- 5.Abdel-Aziz SM, Aeron A, Kahil TA. Health benefits and possiblerisks of herbal medicine. In: Garg N, Abdel-Aziz SM, Aeron A, editors. Microbes in Food and Health. Switzerland: Springer International Publishing; 2016. [Google Scholar]
- 6.Gonnella M, Charfeddine M, Conversa G, Santamaria P. Purslane: A review of its potential for health and agricultural aspects. Eur J Plant Sci Biotechnol. 2010;4:131–6. [Google Scholar]
- 7.Kumar A, Sreedharan S, Kashyap AK, Singh P, Ramchiary N. A review on bioactive phytochemicals and ethnopharmacological potential of purslane (Portulaca oleracea L.) Heliyon. 2022;8:e08669. doi: 10.1016/j.heliyon.2021.e08669. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Iranshahy M, Javadi B, Iranshahi M, Jahanbakhsh SP, Mahyari S, Hassani FV, et al. A review of traditional uses, phytochemistry and pharmacology of Portulaca oleracea L. J Ethnopharmacol. 2017;205:158–72. doi: 10.1016/j.jep.2017.05.004. [DOI] [PubMed] [Google Scholar]
- 9.Popescu C, Popescu C, Manea S, Vladut V, Caba I, Covaliu IC, et al. Study on Portulaca oleracea native species as vegetal source of omega-3 and omega-6 fatty acids. Membranes. 2018;19:21. [Google Scholar]
- 10.Chrysargyris A, Xylia P, Zengin G, Tzortzakis N. Purslane (Portulaca oleracea L.) growth, nutritional, and antioxidant status under different nitrogen levels in hydroponics. Horticulturae. 2024;10:1007. [Google Scholar]
- 11.Yamazaki D, Hitomi H, Nishiyama A. Hypertension with diabetes mellitus complications. Hypertens Res. 2018;41:147–56. doi: 10.1038/s41440-017-0008-y. [DOI] [PubMed] [Google Scholar]
- 12.Castro MM, Tanus-Santos JE. Inhibition of matrix metalloproteinases (MMPs) as a potential strategy to ameliorate hypertension-induced cardiovascular alterations. Curr Drug Targets. 2013;14:335–43. doi: 10.2174/1389450111314030005. [DOI] [PubMed] [Google Scholar]
- 13.Román GC, Jackson RE, Gadhia R, Román AN, Reis J. Mediterranean diet: The role of long-chain ω-3 fatty acids in fish; polyphenols in fruits, vegetables, cereals, coffee, tea, cacao and wine; probiotics and vitamins in prevention of stroke, age-related cognitive decline, and Alzheimer disease. Rev Neurol (Paris) 2019;175:724–41. doi: 10.1016/j.neurol.2019.08.005. [DOI] [PubMed] [Google Scholar]
- 14.Wainstein J, Landau Z, Bar Dayan Y, Jakubowicz D, Grothe T, Perrinjaquet-Moccetti T, et al. Purslane extract and glucose homeostasis in adults with type 2 diabetes: A double-blind, placebo-controlled clinical trial of efficacy and safety. J Med Food. 2016;19:133–40. doi: 10.1089/jmf.2015.0090. [DOI] [PubMed] [Google Scholar]
- 15.Sutjiatmo AB, Suci NV, Bintussolihah F, editors, editors. IOP Conference Series Earth and Environmental Science; IOP Publishing. 2021. Antihypertensive Effects of Purslane (Portulaca oleracea) Extract in Animal Model of Hypertension. [Google Scholar]
- 16.Lee AS, Lee YJ, Lee SM, Yoon JJ, Kim JS, Kang DG, et al. Portulaca oleracea ameliorates diabetic vascular inflammation and endothelial dysfunction in db/db mice. Evid Based Complement Alternat Med. 2012;2012:741824. doi: 10.1155/2012/741824. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17.Moher D, Shamseer L, Clarke M, Ghersi D, Liberati A, Petticrew M, et al. Preferred reporting items for systematic review and meta-analysis protocols (PRISMA-P) 2015 statement. Syst Rev. 2015;4:1. doi: 10.1186/2046-4053-4-1. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 18.Higgins JP, Altman DG, Gøtzsche PC, Jüni P, Moher D, Oxman AD, et al. The Cochrane Collaboration’s tool for assessing risk of bias in randomised trials. BMJ. 2011;343:d5928. doi: 10.1136/bmj.d5928. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 19.Hultcrantz M, Rind D, Akl EA, Treweek S, Mustafa RA, Iorio A, et al. The GRADE Working Group clarifies the construct of certainty of evidence. J Clin Epidemiol. 2017;87:4–13. doi: 10.1016/j.jclinepi.2017.05.006. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 20.Hozo SP, Djulbegovic B, Hozo I. Estimating the mean and variance from the median, range, and the size of a sample. BMC Med Res Methodol. 2005;5:13. doi: 10.1186/1471-2288-5-13. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 21.Borenstein M, Hedges LV, Higgins JP, Rothstein HR. Chichester: Wiley; 2009. Introduction to meta-analysis. [doi: 10.1002/9780470743386] [Google Scholar]
- 22.DerSimonian R, Laird N. Meta-analysis in clinical trials. Control Clin Trials. 1986;7:177–88. doi: 10.1016/0197-2456(86)90046-2. [DOI] [PubMed] [Google Scholar]
- 23.Higgins JP, Thompson SG. Quantifying heterogeneity in a meta-analysis. Stat Med. 2002;21:1539–58. doi: 10.1002/sim.1186. [DOI] [PubMed] [Google Scholar]
- 24.Egger M, Davey Smith G, Schneider M, Minder C. Bias in meta-analysis detected by a simple, graphical test. BMJ. 1997;315:629–34. doi: 10.1136/bmj.315.7109.629. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 25.Sterne JAC, Bradburn MJ, Egger M. Meta-analysis in Stata. In: Egger M, Davey Smith G, Altman DG, editors. Systematicreviews in health care: meta-analysis in context. 6th. London (UK): BMJ Publicing Group; 2005. p. 34772. [Google Scholar]
- 26.Darvish Damavandi R, Shidfar F, Najafi M, Janani L, Masoodi M, Akbari-Fakhrabadi M, et al. Effect of Portulaca oleracea (purslane) extract on liver enzymes, lipid profile, and glycemic status in nonalcoholic fatty liver disease: A randomized, double-blind clinical trial. Phytother Res. 2021;35:3145–56. doi: 10.1002/ptr.6972. [DOI] [PubMed] [Google Scholar]
- 27.Esmaillzadeh A, Zakizadeh E, Faghihimani E, Gohari M, Jazayeri S. The effect of purslane seeds on glycemic status and lipid profiles of persons with type 2 diabetes: A randomized controlled cross-over clinical trial. J Res Med Sci. 2015;20:47–53. [PMC free article] [PubMed] [Google Scholar]
- 28.Gheflati A, Adelnia E, Nadjarzadeh A. The clinical effects of purslane (Portulaca oleracea) seeds on metabolic profiles in patients with nonalcoholic fatty liver disease: A randomized controlled clinical trial. Phytother Res. 2019;33:1501–9. doi: 10.1002/ptr.6342. [DOI] [PubMed] [Google Scholar]
- 29.Papoli M, Pishdad S, Nadjarzadeh A, Hosseinzadeh M. Effects of consuming purslane seed powder on indicators of metabolic syndrome in women: A randomized clinical trial. Prog Nutr. 2019;21:329–35. [Google Scholar]
- 30.Jafari N, Shoaibinobarian N, Dehghani A, Rad A, Mirmohammadali SN, Alaeian MJ, et al. The effects of purslane consumption on glycemic control and oxidative stress: A systematic review and dose-response meta-analysis. Food Sci Nutr. 2023;11:2530–46. doi: 10.1002/fsn3.3311. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 31.Contreras F, Rivera M, Vasquez J, De la Parte MA, Velasco M. Diabetes and hypertension physiopathology and therapeutics. J Hum Hypertens. 2000;14(Suppl 1):S26–31. doi: 10.1038/sj.jhh.1000983. [DOI] [PubMed] [Google Scholar]
- 32.Siriamornpun S, Suttajit M. Microchemical components and antioxidant activity of different morphological parts of Thai wild purslane (Portulaca oleracea) Weed Sci. 2010;58:182–8. [Google Scholar]
- 33.Petropoulos SA, Fernandes Â, Arampatzis DA, Tsiropoulos NG, Petrović J, Soković M, et al. Seed oil and seed oil byproducts of common purslane (Portulaca oleracea L.): A new insight to plant-based sources rich in omega-3 fatty acids. LWT. 2020;123:109099. [Google Scholar]
- 34.Petropoulos S, Karkanis A, Martins N, Ferreira IC. Phytochemical composition and bioactive compounds of common purslane (Portulaca oleracea L.) as affected by crop management practices. Trends Food Sci Technol. 2016;55:1–10. [Google Scholar]
- 35.Clark JL, Zahradka P, Taylor CG. Efficacy of flavonoids in the management of high blood pressure. Nutr Rev. 2015;73:799–822. doi: 10.1093/nutrit/nuv048. [DOI] [PubMed] [Google Scholar]
- 36.Maaliki D, Shaito AA, Pintus G, El-Yazbi A, Eid AH. Flavonoids in hypertension: A brief review of the underlying mechanisms. Curr Opin Pharmacol. 2019;45:57–65. doi: 10.1016/j.coph.2019.04.014. [DOI] [PubMed] [Google Scholar]
- 37.Mazloom Z, Ansar H. The effect of alphalipoic acid onblood pressure in type 2 diabetics. Iran J Endocrinol Metab. 2009;11:245–50. [Google Scholar]
- 38.Boccardi V, Taghizadeh M, Salek M, Jafarnejad S. Blood pressure lowering effects of alpha-lipoic acid supplementation: A meta-analysis of randomized controlled trials. Arterial Hypertens. 2021;25:29–38. [Google Scholar]
- 39.Cabo J, Alonso R, Mata P. Omega-3 fatty acids and blood pressure. Br J Nutr. 2012;107(Suppl 2):S195–200. doi: 10.1017/S0007114512001584. [DOI] [PubMed] [Google Scholar]
- 40.Miller PE, Van Elswyk M, Alexander DD. Long-chain omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid and blood pressure: A meta-analysis of randomized controlled trials. Am J Hypertens. 2014;27:885–96. doi: 10.1093/ajh/hpu024. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 41.Cicero AF, Ertek S, Borghi C. Omega-3 polyunsaturated fatty acids: Their potential role in blood pressure prevention and management. Curr Vasc Pharmacol. 2009;7:330–7. doi: 10.2174/157016109788340659. [DOI] [PubMed] [Google Scholar]
- 42.Floyd ZE, Stephens JM. Controlling a master switch of adipocyte development and insulin sensitivity: Covalent modifications of PPARγ. Biochim Biophys Acta. 2012;1822:1090–5. doi: 10.1016/j.bbadis.2012.03.014. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 43.Bisogni V, Cerasari A, Pucci G, Vaudo G. Matrix metalloproteinases and hypertension-mediated organ damage: Current insights. Integr Blood Press Control. 2020;13:157–69. doi: 10.2147/IBPC.S223341. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 44.Amraoui F, Spijkers L, Hassani Lahsinoui H, Vogt L, van der Post J, Peters S, et al. SFlt-1 elevates blood pressure by augmenting endothelin-1-mediated vasoconstriction in mice. PLoS One. 2014;9:e91897. doi: 10.1371/journal.pone.0091897. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 45.Moreau AG, Savage G. Oxalate content of purslane leaves and the effect of combining them with yoghurt or coconut products. J Food Compos Anal. 2009;22:303–6. [Google Scholar]
- 46.Wang X, Zhang X, Wang L, Zhang R, Zhang Y, Cao L. Purslane-induced oxalate nephropathy: Case report and literature review. BMC Nephrol. 2023;24:207. doi: 10.1186/s12882-023-03236-9. [DOI] [PMC free article] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Random-effects meta-regression plots of the association between mean changes in systolic blood pressure (a and b), and diastolic blood pressure (c and d) and purslane dose and intervention duration
Sensitivity analysis of purslane on diastolic blood pressure (a), and systolic blood pressure (b)
Data Availability Statement
Data will be made available on request.
