Abstract
OBJECTIVE:
Even though oxidative and inflammatory bursts are a big part of renal reperfusion injury (RI/R), Pistia stratiotes (PS) has been used for a long time to stop these overreactions. People have said that it can drop both blood sugar and cholesterol. Hence, the goal of this study was to show how PS changed kidney reperfusion damage in both diabetic and normal rats.
MATERIALS AND METHODS:
In the study, 30 min of renal ischemia (RI) was followed by 1 h of recovery for each rat. Before the test, PS (100 mg/kg p. o.) was given to the animals for 7 days. Then, using the mixture from the separated kidney tissues, the antioxidant, inflammation, and histopathological effects were determined.
RESULTS:
When compared to RI/R, diabetic rats given PS had lower blood sugar, aspartate aminotransferase, blood urea nitrogen, and creatinine, myeloperoxidase, C-reactive protein, and tumor necrosis factor-alpha levels in their urine.
CONCLUSION:
PS potentially worked in hyperglycemic rats protecting them against RI/R. It is possible that PS’s ability to protect the kidneys of the test rats is due to its ability to fight free radicals, lower blood sugar, and stop inflammation.
Keywords: Injury, ischemia, Pistia stratiotes, renoprotective, reperfusion
Introduction
Sschemia is a pathological condition that is distinguished by a reduction in oxygen delivery and an elevation in oxygen requirements within the body. Reperfusion injury is a form of cellular damage that arises from the reversal of ischemia and reperfusion, as documented in literature.[1] Individuals diagnosed with Type 2 diabetes mellitus (T2DM) are more susceptible to experiencing renal complications. Ischemia reperfusion (I/R) during surgical procedures can result in renal damage, leading to necrosis. This is believed to be a significant factor to produce dysfunction and harmful events associated with reduced blood supply to nephrons and causing nephropathy. The present investigation aimed to induce renal reperfusion injury (RI/R) injury in rats with T2DM to gain insights into the pathophysiological mechanisms underlying this disease and to elucidate the potential contribution of augmented inflammatory response to the development of severe (I/R) injury.
The inflammatory response triggered by RI/R injury may cause damage to multiple organs. I/R injury can trigger an inflammatory response that may result in damage to multiple organs. The generation of free radicals and nitric oxide (NO) are significant contributors to the pathophysiological mechanisms underlying I/R injury.[2] The pathogenesis of I/R is significantly influenced by certain inflammatory cells, cell adhesion molecules, and cytokines, as evidenced by previous research.[3] Neutrophils, which are a type of inflammatory cell, are known to generate significant quantities of reactive oxygen species in reaction to I/R injury. The enzyme myeloperoxidase (MPO) is present in neutrophils and is responsible for the production of hypochlorous acid, which is known to cause oxidative damage to cellular components.[4] Insufficient antioxidant defenses facilitate the occurrence of oxidative stress and tissue damage resulting from I/R.
The potential utility of Pistia stratiotes (PS) lies in its possession of secondary metabolites, natural antioxidants, and antibacterial properties. The transport of vital nutrients including calcium, carboxylic acids like super oxide dismutase (SOD), magnesium, zinc, the chlorophyll Vitamin C, as well as DNA, RNA, and proteins is aided by PS’s high level of B-complex vitamins, particularly Vitamin B12.[5] Therefore, it is plausible that PS could serve as a valuable medicinal keystone species.
Materials and Methods
Preparing botanical parts and extracts
The PS plant had been bought from Gujarat University’s Botany Department of the Faculty of Science, and a taxonomist’s certification. The PS specimen had undergone desiccation and exhibited a state of sterility. Using a Soxhlet apparatus, 200 cc of 95% ethanol was used to extract the dry powder at 50°C. After that, the mixture was set aside until it reached 72°C. The desiccated extract was stored in a hermetically sealed receptacle and maintained under optimal temperature and humidity conditions.[6]
Phytochemical evaluation
Examination revealed the presence of phenols, proteins, terpenoids, flavonoids, alkaloids, and saponins.
Phenolic content
By applying the FolinCiocalteu (FC) reagent, ascertain the total phenolic content. Plant extract and FC reagent were combined and incubated at 22°C for 5 min. The FC reagent was diluted 1:1 with distilled water. Then, 2 mL of 20% Na2CO3 were introduced. The combination was then incubated at 22°C for another 90 min before its absorbance at a wavelength of 650 nm was measured. Acid was utilized as a reference to quantify the overall phenolic content (mg/mL).
Flavonoid content
The aluminum chloride (AlCl3) technique was deployed to determine the total amount of flavonoids (mg/mL). 0.5 ml of the plant extract, 0.5 ml of water, and 0.3 ml of 50 sodium nitrite made up the assay mixture, which underwent a 5-min incubating at 25°C. The following, 0.3 ml of 10% AlCl3 and 1 or 2 ml of 1 M NaOH were added to the reaction mixture. In conclusion, absorbance is measured at the wavelength of 510 nm was calculated employing quercetin as a reference.
Alkaloids content
2 mL of hexane and 0.5 mL of plant extract were combined, well agitated, and then filtered. The plant extract was then given 3 mL of 2% hydrochloric acid. The reaction mixture was additionally heated and filtered. Upon mixing the filtrate and a minute quantity of acid, an obvious formation of a yellow precipitate was observed, thereby indicating the presence of alkaloids.
Terpenoids content
Three milliliters of extract were combined with 1 ml of chloroform and 1 ml of strong sulfuric acid to produce the deep reddish-brow coloration that shows the presence of terpenoids.
Experimental design and surgical procedure
The experimental animal employed in this study was a male Sprague-Dawley rat weighing between 250-300 grams. The rat was acclimated to a polypropylene cage and maintained at a temperature of 22°C. The lighting conditions consisted of a half-day light and dark phase. The Institutional Animal Ethics Committee approved this procedure, which followed CPCSEA criteria (PIPH 16//18921//PO//ReBi//S/05/CPCSEA). Six normal rats made up Group 1 (n = 1), which underwent all surgeries without obstructing the renal artery; Group 2 (n = 6) consisted of diabetic rats. Group 3 (n = 6): (RI/R), renal arteries were obstructed for 30 min and reperfused for an hour; Group 4 (n = 6) Diabetic Rats undergoes Renal ischemia Reperfusion Injury (DRI/R), after diabetes onset, had a half-hour-hour renal artery blockage and 1-h reperfusion; Group 6: PS-treated diabetic rats (DPS) received PS (100 mg/kg p. o.) for 1 week before having their renal arteries occluded for 30 min and reperfused for an hour on day 7. Blood sugar levels, food and water consumption, weight gain, and weight loss were evaluated using Sigma Aldrich Pvt. Ltd diagnostic kits to assess diabetes severity.[7] Rats with diabetes and healthy rats were both put unconscious after 4 weeks with ketamine (60 mg/kg i. p.) and diazepam (5 mg/kg). The method maintained 37 0.5°C blood temperature. A midline incision revealed diabetic and healthy rats’ left and right renal pedicles.
The induction of renal ischemia (RI) was achieved by the application of bilateral renal pedicle clamping for a duration of 30 min. Following the release of the clamp, the renal system was observed for a duration of 24 h. The rats were euthanized, and their kidneys were extracted and preserved in nitrogen at a temperature of 70°C until further analysis of their oxidant and antioxidant parameters was conducted.[8] The rats received nicotinamide adenine dinucleotide (NAD) at a dose of 230 mg/kg i. p, for 15 min after receiving streptozotocin at a dose of 65 mg/kg iv for a period of 7 days to induce diabetes. For the aim of monitoring diabetes, Beacon Pvt. Limited’s regular diagnostic kits were used to assess blood sugar levels, weight growth, food intake, and water intake.[9]
Renal performance
With industry-standard test kits by Span Diagnostics in Gujarat, an Indian state, samples of serum were examined for blood urea nitrogen (BUN) (using Jaffe’s colorimetric approach), creatinine (using the DAM technique), and aspartate aminotransferase (AST).[10]
Oxidative stress and inflammatory response biomarkers
The current study measured lipid peroxidation levels in renal tissue (NO), as indicated by Malondialdehyde (MDA) concentration, as well as intrinsic antioxidant enzymes such as reduced glutathione (GSH),[11] SOD,[12] catalase (CAT),[13] GSH peroxidase (GSHPx),[14] and xanthine oxidase (XO).[15] Tumor necrosis factor (TNF−) and C-reactive protein (CRP) levels in the blood were measured using kits procured from Nicholas Pvt. Ltd. in India. The current work seeks to investigate the activity of MPO[16] as well as the amount of neutrophil infiltration in renal tissue.
Histological analysis and DNA fragmentation
A histological examination of the paraffin-embedded kidneys was conducted. In order to mount these segments on albumin-coated glass slides, we cut thin slice 5 μm thick with a microtome. Following a brief period of eosin staining and a series of escalating alcohol solutions, the hematoxylin-stained sections were affixed to Canada balsam. Stained slices were captured using an Olympus BX40 photomicroscope. The samples were evaluated by an experienced pathologist or through a blinded study in order to identify any histological alterations. Each kidney slide was subjected to the review of a minimum of 10 fields, and any changes observed were graded as either none (−), mild (+), moderate (++), or severe (+++). With the aid of a DNA extraction kit, genomic DNA was extracted from renal tissue. A voltage of 80 volts was used for electrophoresis for 1–2 h. We observed under ultraviolet light the DNA ladders that resulted from the fragmentation of nucleosome DNA in tissues that have been undergoing apoptosis, and we documented them for future reference.[17,18]
Statistical analysis
To represent all of the values, the mean standard error of the average (standard error of mean) was used. A computer-based tool (GraphPad, Software, 225, Franklin.Street.Fl.26Boston, MA02110) was used to execute the Bonferroni multiple comparisons test after one-way ANOVA to determine the statistical significance of two groups, where P = 0.05 was used as the significance level.
Results
Effect of Pistia stratiotes on diabetic markers
During the experiments, various parameters were recorded including body weight, food and drink intake, blood sugar and insulin levels, RI and reperfusion in Normal Sham Operated (NSO) and Diabetic Sham Operated (DSO) rats, Normal animals treated with Pistia stratiotes (NPS) and Diabetic animals treated with Pistia stratiotes (DPS) rats, as well as RI/R in normal along with diabetic rats. These data were documented using the DPS method [Table 1].
Table 1.
Effect of Pistia stratiotes on diabetic markers (n=6)
| Groups | NSO | DSO | R/IR | DR/IR | NPS | DPS |
|---|---|---|---|---|---|---|
| Body weight (g) | 279.81±20.07 | 172.7±20.1 | 221.46±17.30 | 174.41±21.37 | 196.34±12.25# | 184.45±11.53@ |
| Food intake (g/animal/day) | 22.06±2.01 | 25.87±2.58 | 14.87±1.77 | 10.62±2.23@ | 21.75±2.18*,@ | 27.91±7.91 |
| Water intake (mL/animal/day) | 19.12±3.31 | 44.5±6.16 | 16.5±4.31 | 52.14±8.77 | 30.62±6.59* | 39.71±16.1 |
| Serum glucose (mg/dL) | 101.75±29.43 | 378.62±22.45 | 114.37±6.96 | 323.41±31.32 | 122.37±8.56@ | 134.67±9.73 |
| Serum insulin (µU/mL) | 39.87±4.86 | 76.87±12.32* | 56.35±4.59 | 84.5±11.21 | 46.12±6.78# | 41.94±10.3 |
Values are mean ± SEM (n = 6), analyzed by one-way ANOVA followed by Bonfferoni’s multiple comparison tests. *denote (P < 0.05) for chance differences vs NSO, #denote (P < 0.05) for chance differences vs DSO, @denote (P < 0.05) for chance differences vs RI/R in Body Weight, Food Intake, Water intake, Serum Glucose and serum insulin. Values are mean±SEM (n=6), analyzed by one-way ANOVA followed by Bonfferoni’s multiple comparison tests. SEM=Standard error of mean, DPS=Pistia stratiotes - treated diabetic rats, R/IR=Renal reperfusion injury, NSO = Normal sham operated, DSO = Diabetic sham operated, NPS=Normal sham operated, DP=Diabetic rats Treated with Pistia stratiotes, DR/IR=Diabetic renal ischemia reperfusion injury
Pistia stratiotes’s effect on renal function
Higher blood levels of AST, BUN, and C-Reactive Protein (CRP) were discovered in diabetic rats given RI/R than in diabetic animals who underwent sham surgery, indicating glomerular dysfunction. The blood concentrations of AST, BUN, and CTN varied between the RI/R and DRI/R groups as well. Compared to the RI/R and DRI/R groups, PS therapy decreased the levels of AST, BUN, and creatinine [Figure 1].
Figure 1.
Effect of Pistia stratiotes on renal health as determined by (a) aspartate aminotransferase, (b) blood urea nitrogen, and (c) creatinine. The values are mean standard error of mean (n = 6), and they were evaluated using one-way ANOVA and Bonfferoni’s multiple comparison tests. *(P < 0.05) difference in chance versus NSO, #(P < 0.05) difference in chance versus DSO, @(P < 0.05) difference in chance versus RI/R, and $(P < 0.05) difference in chance versus DR/IR rats. AST = Aspartate aminotransferase, BUN = Blood urea nitrogen, NSO = Normal sham operated, DSO = Diabetic sham operated, R/IR = Normal renal ischemia reperfusion injury, DR/IR = Diabetic renal ischemia reperfusion injury, NPS = Normal animals treated with Pistia stratiotes, DPS = Diabetic animals treated with Pistia stratiotes
Pistia stratiotes’s effect on oxidative stress markers
Quality factor and DRI/R rats had considerably greater MDA and XO levels than NSO and DSO rats. The RI/R and DR/IR rat groups had lower GSH, GSHPx, CAT, and SOD activity than the NSO and DSO groups. PS therapy substantially reduced MDA and XO levels and increased GSH, GSHPx, CAT, and SOD activity compared to RI/R [Figure 2].
Figure 2.
After renal reperfusion injury (RI/R) in NSO, DSO, and Pistia stratiotes -treated rats, the following changes were observed in the renal tissue: Catalase (a); MDA (b); glutathione (c); GSH peroxidase (d); super oxide dismutase (e); and xanthine oxidase (f). Values are mean standard error of mean (n = 6), and one-way ANOVA analysis is followed by multiple comparison tests by Bonfferoni. For chance variations compared to NSO, *(P < 0.05), #(P < 0.05), @(P < 0.05), for chance variations compared to RI/R, and $(P < 0.05) for chance variations compared to DR/IR rats. CAT = Catalase, GSH = Glutathione, GSHPx = GSH peroxidase, XO = Xanthine oxidase, NSO = Normal Sham Operated, MDA = Malondialdehyde, DSO = Diabetic Sham Operated, R/IR = Normal renal ischemia reperfusion injury, DR/IR = Diabetic renal ischemia reperfusion injury, NPS = Normal animals treated with Pistia stratiotes, DPS = Diabetic animals treated with Pistia stratiotes
Pistia stratiotes’s effect on nitric oxide levels and Inflammatory mediators in renal reperfusion injury
We found that NO levels in the RI/R and DRI/R groups were significantly greater than those in the NSO and DSO groups, but NO levels were substantially lower in the PS group presented than those in the RI/R and DRI/R groups. The MPO levels in the RI/R and DRI/R group of rats were observed to be significantly higher in comparison to the NSO and DSO Group, whereas the PS-treated rats exhibited a marked decrease in MPO levels. The rats with RI/R or DRI/R exhibited markedly higher amounts of CRP compared to those that received treatment with NSO or DSO. However, the CRP levels of the former group were still significantly lower than those of the rats that received treatment with PS. The TNF levels observed in rats subjected to RI/R and DRI/R exhibited a statistically significant increase in comparison to the NSO and DSO groups. However, these levels were significantly lower than those observed in rats treated with PS. The observed discrepancy exhibited statistical significance [Figure 3].
Figure 3.
Following renal reperfusion injury (RI/R) in healthy, diabetic, and Pistia stratiotes -treated rats, renal tissue nitric oxide levels, C-reactive protein, myeloperoxidase, and serum tumor necrosis factor-α levels were measured. Values are mean standard error of mean (n = 6), and one-way ANOVA analysis is followed by multiple comparison tests by Bonfferoni. For chance discrepancies vs. NSO, use * to signify (P < 0.05), and for chance discrepancies versus RI/R rats, use @ to signify (P < 0.05). MPO = Myeloperoxidase, NO = Nitric oxide, TNF = Tumor necrosis factor, NSO = Normal sham operated, DSO = Diabetic sham operated, R/IR = Normal renal ischemia reperfusion injury, DR/IR = Diabetic renal ischemia reperfusion injury, NPS = Normal animals treated with Pistia stratiotes, DPS = Diabetic animals treated with Pistia stratiotes
Pistia stratiotes’s effect on renal histology and DNA fragmentation
When contrasted with (A) and (B), photomicrographs of kidney tissues colored with eosin and hematoxylin at 10 times from the I/R groups revealed lymphocytic proliferation and necrosis of nephrons. PS treatment significantly reversed damage in experimental rats, as shown in (E) and (F). The cortical tubules showed the most dramatic alterations, with histological damage ranging from healthy (NSO and DSO categories) to moderate (RI/R group) to serious (DRI/R + RI/R group). Histopathological changes were rated and summarised for the reader [Table 2]. The RI/R control, DRI/R, NPS, and DPS groups exhibited the characteristic DNA laddering activity, indicative of cellular apoptosis. In contrast to RI/R group, the PS treated group showed less DNA fragmentation and apoptosis, as shown in rats [Figure 4].
Table 2.
Effect of Pistia stratiotes on renal histology (n=6)
| Groups | Tubular cell swelling | Interstitial edema | Tubular dilatation | Necrosis of epithelium | Hyaline casts |
|---|---|---|---|---|---|
| NSO | − | − | − | − | − |
| DSO | − | − | − | − | − |
| RI/R | ++ | ++ | ++ | ++ | ++ |
| DRI/R | +++ | +++ | +++ | +++ | +++ |
| NPS | + | + | − | − | − |
| DPS | + | + | − | − | − |
Effect of EC on morphological changes of kidneys (n=6), as assessed by histopathological examination of the normal rats, and diabetic rats exposed to RI/R. DPS=Pistia stratiotes - treated diabetic rats, R/IR=Renal reperfusion injury, NSO = Normal sham operated, DSO = Diabetic sham operated, PS=Pistia stratiotes, NPS=Normal animals treated with Pistia stratiotes, DP=Diabetic rats Treated with Pistia stratiotes, DRI/R=Normal renal ischemia reperfusion injury
Figure 4.
The fragmentation of DNA testing revealed typical DNA fragment laddering. (1) Standard Protein Sequence (2) NSO; (3) DSO; (4) RI/R; (5) DRI/R; (6) NPS subjected to RI/R; and (7) DPS The diabetic rats were treated with Pistia stratiotes (PS) and subjected to RI/R. Renal tissue slices from normal and diabetic rats that were treated to RI/R were examined under a BIOXL light microscope to look for morphological alterations. Hematoxylin and eosin (×40) was used to capture images under light microscopy: are shown in (a-c and e), respectively. (d) are shown in (a e and f),respectively. (f) PS Took care of the diabetic rat’s nephro ischemia reperfusion. NSO = Normal sham operated, DSO = Diabetic sham operated, R/IR = Normal renal ischemia reperfusion injury, DR/IR = Diabetic renal ischemia reperfusion injury, NPS = Normal animals treated with Pistia stratiotes, DPS = Diabetic animals treated with Pistia stratiotes
Discussion
Numerous pharmaceuticals currently available are being utilized or explored for their potential nephroprotective effects in the treatment of RI/R. Regrettably, a majority of these treatments did not demonstrate significant therapeutic responses because of a range of patient, and drug-related circumstances. New pharmaceuticals are currently in development to hinder various mechanisms which have been associated with the onset of stroke, including the kidneys apoptosis, inflammatory conditions, and angiogenesis.
The present study posited that the administration of PS would confer protection to rats in the context of a standard rat model of RI/R and DRI/R. In the context of nephrological conditions, PS is employed as a means to mitigate the impact of oxidative stress, inflammation, hyperglycemia, and tissue damage resulting from ischemia, as documented in reference.[12] Through examination of the concentrations of enzymes that neutralize free radicals, and NO in kidney tissue, the study sought to determine the degree of oxidative injury and the protective effects of PS. The current study observed a notable improvement in renal function among rats that were subjected to RI/reperfusion and treated with PS.
Transient RI is widely acknowledged to be linked with nephrological abnormalities. The findings indicate that PS provides renal protection against the damage caused by arterial renal occlusion-induced RI/R injury. The red formazan pigment is produced from Triphenyl tetrazolium chloride (TTC) through the catalytic action of dehydrogenase and NAD within living cells. Real-time cell imaging was utilized to observe the manifestation of red staining. Cells that have undergone infarction exhibit a deficiency in these particular enzymes, resulting in a lack of staining and a dull yellow appearance.[19] The present study exhibited the presence of a red kidney region in rats that underwent treatment, thereby providing substantiation of the protective properties of PS treatment against RI/R. The RI/R and DRI/R groups were subjected to histopathological examination, which revealed significant constriction of blood vessels, infiltration of neutrophils, and necrosis of nephrons. The PS-treated group exhibited significantly reduced neutrophil infiltration in equated to the RI/R and DRI/R groups.
NO plays a crucial role as a messenger or modulator,[20] although it can be detrimental in certain circumstances, such as oxidative stress. RI induces the overproduction of NO via various contributing factors. The chemical mechanism of oxidative stress resulting from augmented NO production due to RI/R was elucidated by the highly reactive ONOO,[21] The study’s findings indicate that the levels of NO in rats treated with PS were significantly lower compared to the RI/R and DRI/R groups. The groups that received PS treatment exhibited a decrease of 16.37% in NO levels.
The findings indicate a significant increase in the activities of lactoperoxidase, XO, and NO. The lowered action of enzymes that detoxify free radicals in the RI/R groups provide evidence for the kidney damage caused by oxidative stress. The groups that received PS treatment showed a considerable shoot up in both CAT and SOD levels, with a respective rise of 19.67% and 22.14%. The findings indicate that the PS-treated groups exhibited a statistically significant increase in GSH levels, surpassing those of the RI/R-treated groups by 31.2%. The groups that received PS treatment exhibited an increase of 18.37% in GSHPx levels. The findings presented here contradict those of a prior study, which indicated that an overabundance of oxygen species leads to an increase in lipid peroxidation and NO, while simultaneously reducing the activity of superoxide dismutase, CAT, XO, GSHPx, and GSH. This is thought to occur as a result of the deactivation of detoxification mechanisms and the breakdown of antioxidants.[22]
The MPO enzyme induces molecular radicalization, leading to the activation of apoptosis and protein nitrotyrosination, as documented in reference.[23] A notable disparity in MPO levels was observed between the group with ischemia and the group serving as the control. The conclusions of this study show that, when compared to the RI/R as well as DRI/R groups, the administration of PS therapy resulted in a statistically significant decrease in MPO values. The groups that received PS treatment exhibited a decrease of 20.96% in MPO levels.
The quantity and potency of pro-inflammatory cytokines in the serum may escalate in reaction to elevated levels of CRP. The study demonstrated a swift elevation in serum CRP levels subsequent to RI. This finding is noteworthy as CRP serves as an indicator for evaluating the gravity, prognosis, and relapse of stroke.[24] The findings indicate a statistically significant decrease in CRP levels among the PS treatment group in comparison to the RI/R and DRI/R groups. The groups treated with PS exhibited a reduction of 22.13% in CRP levels.
The production of TNF, whether internal or driven on by acute RI, is a major factor in the development of renal damage. The induction of TNF following RI may lead to the aggregation and activation of multicore white blood cells, as well as the production of inflammatory mediators. This has been documented in previous research.[25] The administration of comparing the PS group to the RI/R along with DRI/R groups, the serum TNF levels significantly dropped by 24.48%. A possible indicator of PS therapy’s effectiveness is the restoration of normal blood flow and blood pressure, possibly attributable to a decrease in the values of renin release.
Procaspases 3 and 9 are activated by the discharge of cytochrome within the cytosol, which eventually causes the development of the apoptosome. The activation of caspase 3 leads to the activation of caspase triggered DNase,[26,27] which ultimately results in the fragmentation of DNA. In addition, it was ascertained that apoptosis transpires in RI/R animals’ renal more frequently. In contrast to NSO rats, or DRI/R rats in compared to DSO rats. The findings of the study indicate that the administration of PS resulted in a reduction of DNA fragmentation in both the NPS and DPS groups. This suggests that there was a decrease in nuclear oxidative stress in the renal tissue of diabetic rats before RI/R.
The findings indicate that PS exhibited a preventive effect against RI/R in rats with diabetes. The potential renoprotective advantages observed in the experimental animals could be ascribed to the antioxidant, blood sugar-reducing, and membrane-stabilizing properties of PS. Further investigation is required to fully capitalize on the therapeutic potential of PS in renovascular diseases, due to the unique concepts raised by the results.
Conclusion
In conclusion, it was discovered that PS was successful in preventing RI/R in diabetic rats. In addition, the antioxidant, blood sugar-lowering, and membrane-stabilizing activities of PS may be responsible for the renoprotective effect shown in experimental animals. In order to make use of the full therapeutic potential of Pistia stratiotes in the treatment of Renovascular illnesses, more research must be conducted to follow novel possibilities that are developing as a consequence of these breakthroughs.
Contributions from authors
Shantilal Padhiyar interpreted the info, drafted, and revised the manuscript. Jitendra vaghasiya, Vashisth P Bhavsar, and Ashish Patel contributed to the analysis and interpretation of knowledge. Tejas B Patel and Vashisth Bhavsar contributed to the work’s planning and modification. The submitted paper’s final draft has been examined and endorsed by all authors.
Ethics approval and consent to participate
Weighting between 250 and 300 g, male Sprague-Dawley rats were subjected to acclimatization within a polypropylene cage under controlled conditions of 22°C ± 3°C temperature and a 12-h period of light and darkness. The Institutional Animal Ethical Committee approved this procedure (No PIPH 16//18921/PO/ReBi//S/05/CPCSEA) and executed in accordance with the regulations of CPCSEA.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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