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. 2026 Apr 8;7(2):154–162. doi: 10.14744/hf.2025.98035

A traditional herbal remedy in liver diseases: Momordica charantia L. (kudret narı/bitter melon)

Dudu Altintas Gunduz 1,✉, Yasemin Balaban 2, Ufuk Koca Caliskan 1,3
PMCID: PMC13442721  PMID: 42564386

Abstract

The liver is the central organ regulating the body’s metabolism; therefore, liver diseases negatively affect metabolic activities as well as the immune system. Momordica charantia L. is one of the medicinal plants used in folk medicine to prevent or treat liver diseases. M. charantia contains compounds with antioxidant and anti-inflammatory properties that protect liver cells from free radical damage and reduce inflammation. In addition, the phytochemicals of M. charantia may help regulate blood sugar levels, thereby supporting metabolism and reducing fat accumulation in the liver. Previous studies indicate that M. charantia has the potential to enhance liver function while reducing the incidence of fatty liver disease. This study aimed to summarize data from in vivo studies investigating the hepatoprotective mechanisms of M. charantia at various application doses, highlighting its potential as a future dietary supplement candidate. However, due to insufficient evidence regarding its safety, the possibility of hepatotoxic effects should not be disregarded.

Keywords: Bitter melon, hepatoprotective effect, liver diseases, Momordica charantia, non-alcoholic fatty liver disease (NAFLD)

Points to Note

  • Synthesis of Current Evidence: This review examines whether bitter melon (Momordica charantia) has hepatoprotective effects.

  • Major Controversies: Preclinical studies show M. charantia improves fatty liver, alcohol-related liver injury, and hepatocellular damage through antioxidant, anti-inflammatory, and lipid-lowering effects, though clinical evidence is limited.

  • Future Directions: Bitter melon may support liver health, but it should not be routinely recommended due to insufficient human trials, dosing, and safety data.

Introduction

The liver is responsible for several vital functions, including detoxification, protein synthesis, the bile production and secretion, glucose metabolism, bilirubin metabolism, blood clotting, and control of immune function.[1] Several diseases and conditions are frequently associated with liver dysfunction, including hepatitis A, hepatitis B, hepatitis C, hepatitis E, alcohol-related liver diseases, autoimmune hepatitis, non-alcoholic fatty liver disease (NAFLD), drug-induced liver injury, and hepatocellular carcinoma.[2] Given the rising prevalence of liver diseases, there is an increasing need to identify plants and plant-derived compounds that can provide hepatoprotective benefits. Studies indicate that green tea, resveratrol, milk thistle, garlic, and artichoke are among the plants that demonstrate hepatoprotective properties.[3] Although these plants exhibit hepatoprotective effects, they may also become hepatotoxic when consumed in excessive amounts. Green tea, for instance, can induce hepatotoxicity due to its content of epigallocatechin gallate (EGCG). The safe dose of EGCG has been established as less than 338 mg per day. When this threshold is exceeded, EGCG may trigger oxidative damage and potentially lead to mutations.[4] The use of herbs in maintaining human health has a history spanning several centuries. In recent years, there has been a significant increase in interest in the potential of medicinal plants for the protection and enhancement of liver health.

The fruits of Momordica charantia L. have been traditionally used for the prevention or treatment of liver diseases, particularly in Asian countries.[5] Therefore, this study focuses on investigating the hepatoprotective effects of M. charantia. Due to the limited number of clinical studies evaluating the hepatoprotective effects of M. charantia, the present study primarily focuses on evidence from in vivo and in vitro experiments. Although M. charantia has been used medicinally for a long time, recent studies suggest that the alpha-momorcharin compound isolated from its seeds may cause toxicity.[6] In addition, triterpenic compounds, namely 22-hydroxy-23,24,24,25,26,27-pentanorcucurbit-5-en-3-one and 3,7-dioxo-23,24,25,26,27-pentanorcucurbit-5-en-22-oic acid, isolated from M. charantia stems, have also been shown to cause toxicity in the HepG2 cell line.[7]

Search Strategy

Electronic literature sources were used to prepare this narrative review. The keywords Momordica charantia, bitter gourd, hepatoprotective effect, bitter melon, liver health, preclinical studies, and clinical studies were searched in the PubMed®, Scopus, Web of Science, Google Scholar, and EBSCOhost databases and combined using the search terms “AND,” “OR,” and “NOT.” As the study focused on hepatoprotective effects, other liver diseases were not included. Database searches were updated weekly. Clinical trials and in vivo studies were primarily included. As this research is a narrative review, no formal assessment of study quality was performed.

M. charantia

M. charantia, commonly known as “bitter melon” or “bitter gourd,” is a species belonging to the Cucurbitaceae family. M. charantia has a long history of use in traditional medicine for the treatment of various conditions, including anemia, diabetes, intestinal parasites, digestive system diseases, skin wounds, and liver diseases.[5] In Turkish traditional medicine, an oily macerate prepared by soaking the fruits in olive oil is used to treat gastrointestinal disorders and as a wound-healing agent.[8] In India, the fruits have been traditionally used for various therapeutic purposes, including the treatment of diabetes, psoriasis, and scabies, as well as for their abortifacient and antihelmintic effects.[9] M. charantia fruits are also frequently used for the treatment of jaundice in India.[10]

The pharmacological efficacy of M. charantia has been demonstrated in scientific studies investigating its diverse chemical composition and traditional medicinal uses. These studies have examined its analgesic effect,[11] antidiabetic activity,[12] anti-inflammatory activity,[13] hepatoprotective activity,[14] hypolipidemic effect,[15] and wound-healing activity.[16] The present study aims to review the literature on hepatoprotection, which is defined as the ability of a substance or treatment to protect the liver from damage or disease (Table 1).

Table 1.

Phytochemical constituents identified in different parts of Momordica charantia L.

Plant part Chemical components Chemical groups
Root Quercetin[17] Flavonoid
Kaempferol[17] Flavonoid
Catechin[17] Flavonoid
Chlorogenic acid[17] Flavonoid
Momordicoside X Cucurbitane-type triterpene saponin
3β, 7β, 25-trihydroxycucurbita-5 23(E)-dien-19-al[18] Cucurbitane-type triterpene saponin
Momordicin I[18] Cucurbitane-type triterpene saponin
Momordicin II[18] Cucurbitane-type triterpene saponin
Kuguaglycoside G[18] Cucurbitane-type triterpene saponin
Leaves Caffeic acid[19] Phenolic compounds
Gallic acid[19] Phenolic compounds
Chlorogenic acid[19] Phenolic compounds
Karavilagenin F[20] Cucurbitane-type triterpene saponin
Karaviloside XII[20] Cucurbitane-type triterpene saponin
Karaviloside XIII[20] Cucurbitane-type triterpene saponin
Momordicine VI[20] Cucurbitane-type triterpene saponin
Momordicine VII[20] Cucurbitane-type triterpene saponin
Momordicine VIII[20] Cucurbitane-type triterpene saponin
(19R,23E)-5β,19-epoxy-19-methoxycucurbita-6,23,25-trien-3β-ol[20] Cucurbitane-type triterpene saponin
Kuguacin R[20] Cucurbitane-type triterpene saponin
Fruits Lycopene[21] Carotenoids
β-carotene[21] Carotenoids
Zeaxanthin[21] Carotenoids
Lutein[21] Carotenoids
Charantadiol A[22] Triterpene saponin
Charantagenin E[22] Triterpene saponin
Stigmasterol[22] Sterols
7,25-dihydroxycholesterol[22] Sterols
Goyaglycoside B[22] Triterpene saponin
Charantagenin D[22] Triterpene saponin
Kuguaglycoside C[22] Triterpene saponin
Momordicoside K[22] Triterpene saponin
Quinic acid[23] Phenolic compounds
Benzoic acid[23] Phenolic compounds
Gallic acid[23] Phenolic compounds
Seeds α-eleostearic acid (45.60%)[24] Fatty acids
Stearic acid (28%)[24] Fatty acids
Oleic acid (12.45%)[24] Fatty acids
Linoleic acid (8.90%)[24] Fatty acids
trans-Nerolidol (61.6%)[25] Sesquiterpene
Apiole (8.9%)[25] Phenylpropene
cis-Dihydrocarveol (4.9%)[25] Monoterpenoids
Germacrene D (4.4%)[25] Sesquiterpene
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The plant is a rich source of phytochemicals, consisting of various phytochemical groups found in different parts of the plant in varying concentrations. It has been demonstrated that the roots of M. charantia contain a variety of phenolic compounds, including flavonoids and triterpene saponins (Fig. 1).[7]

Figure 1.

Figure 1

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Molecular structure of M. charantia components (illustrated by the authors).

Non-Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease has been reclassified under the umbrella term steatotic liver disease. Metabolic dysfunction-associated steatotic liver disease is the new name for the liver disease formerly known as NAFLD.[34] In recent times, there has been an alarming rise in the prevalence of NAFLD, which in now considered one of the most common forms of liver disease, affecting approximately 25% of the global population. The incidence of this disease is closely associated with the increasing prevalence of obesity.[35] NAFLD is a broad category that encompasses a spectrum of conditions ranging from simple steatosis (hepatic steatosis) to inflammation (steatohepatitis), with or without fibrosis, known as non-alcoholic steatohepatitis (NASH). Additionally, evidence suggests that NAFLD is associated with the development of cirrhosis and hepatocellular carcinoma (HCC).[36]

In a study utilizing a mouse model of NAFLD, the effect of M. charantia extract on the progression of NAFLD was examined following the administration of a high-fat diet for five days. When the experimental and control groups were compared, blood glucose, cholesterol, and low-density lipoprotein levels were found to decrease in the experimental group fed a high-fat diet. Histological examinations also revealed improvements in liver structure and function.[37] In a further study, the efficacy of M. charantia compounds on the liver was evaluated by isolating the triterpenic saponins 3β, 7β, 25-trihydroxycucurbita-5,23(E)-dien-19-al and momordicine II, which were observed to inhibit lipid accumulation in HepG2 cells.[38]

The impact of protein derived from M. charantia fruits on NAFLD was examined in both in vitro and in vivo assays. It was observed that pretreatment of HepG2 cells with this isolated protein protected them from cellular changes such as steatosis. It was also demonstrated that intracellular triglyceride levels decreased and bile acid production increased. In addition, while findings such as liver discoloration and swelling were observed in rats fed a high-fat diet, lipid accumulation was significantly reduced and no hepatocyte growth was observed in the groups that received M. charantia protein at doses of 400 and 800 mg/kg.[39]

The effect of M. charantia juice on NAFLD development was investigated in mice at doses of 0.5 and 5 g/kg. In the M. charantia-treated group, kidney fat mass and liver weight were significantly lower than those in the fat-only diet group (p<0.05).[40]

Alcohol-Related Liver Disease

Chronic alcohol consumption can result in a range of liver damage, from fatty liver with microvesicular steatosis to cirrhosis and HCC. Furthermore, alcohol consumption has been shown to induce mitochondrial DNA damage in hepatocytes.[41] As the duration of alcohol consumption increases, there is a corresponding increase in lipid accumulation in hepatocytes, along with the activation of inflammatory damage, fibrogenesis, and carcinogenesis pathways.[42]

An 80% ethanol extract prepared from M. Charantia fruits was investigated for its protective effects against alcohol-induced liver damage in mice. The results of the analyses indicated a statistically significant reduction in liver weight and in the levels of alanine aminotransferase and aspartate aminotransferase, which are biochemical markers of liver damage (p<0.05). Histological examinations also demonstrated a reduction in lipid accumulation within hepatocytes.[43]

Hepatocellular Carcinoma

Hepatocellular carcinoma is the most common primary liver cancer and its incidence is increasing. Diseases such as hepatitis B, hepatitis C, and NASH, as well as alcohol consumption, have been implicated in its etiology. Cirrhosis is known to be one of the strongest risk factors for HCC.[44]

A lectin isolated from M. charantia was investigated using in vitro and in vivo methods. In a study conducted using the HepG2 cell line, increased apoptosis was observed at higher doses (p<0.01). Histological evaluations in mice also revealed a significant decrease in tumor volume (p<0.01).[45]

Cucurbitan-type saponosides extracted from M. charantia fruits were assessed for their antiproliferative effects on Hep3B and HepG2 liver cell lines. The half maximal inhibitory concentration (IC50) values for caraviloside III were determined to be 16.68 µM for Hep3B and 4.12 µM for HepG2, indicating that it is the most effective saponoside. The IC50 values for 5-fluorouracil, which was used as the positive control, were determined to be 15.49 µM for Hep3B and 33.58 µM for HepG2.[46]

The in vitro and in vivo effects of Momordica anti-HIV protein of 30 kDa (MAP30) protein, isolated from M. charantia seeds, were evaluated in cancer cells. In vitro studies demonstrated that the compound induced cell cycle arrest at the S phase in the HepG2 cell line. In a mouse model of liver cancer, a dose of 2 mg/kg of MAP30 was administered every two days. Consequently, a notable reduction in tumor volume and size was observed, as confirmed by histological analysis (p<0.05).[47]

The oral administration of M. charantia seed oil to rats yielded statistically significant outcomes. These included a reduction (p<0.05) in the mean number, diameter, and area of dysplastic nodules in the liver, as well as a reduction in the size of neoplastic lesions compared to the control group.[48]

Hepatoprotective Mechanisms of M. charantia

The use of plants in natural medical treatments has a long history spanning thousands of years. Advances in science and technology have enabled the efficacy and safety of herbal products to be studied in greater detail, and these products are now available in a variety of formulations. Formulation development is a crucial step in enhancing the efficacy of herbal products while reducing their potential adverse effects on the human body. The components of each herbal product may have different mechanisms of action; therefore, it is necessary to determine how these components can be used most effectively.[49]

Given that herbal extracts contain complex mixtures of phytochemicals, they exhibit a wide range of pharmacological effects through various mechanisms. Hazardous agents such as alcohol can damage hepatocytes and impair the normal functioning of their membranes. Consequently, the activities of transaminases and alkaline phosphatase increase as a result of this damage.[50]

Chronic alcohol consumption can lead to lipid oxidation, resulting in the disruption of membrane permeability. This process involves the formation of hydroxylethyl radicals, which primarily target polyunsaturated fatty acids. Certain fractions of M. charantia have been shown to maintain the membrane integrity of liver cells by inhibiting alcohol-induced lipid peroxidation in the liver.[31] The oxidative mechanism is illustrated in Figure 2.[51]

Figure 2.

Figure 2

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Antioxidant effect mechanism of M. charantia (original creations). The effectiveness of Momordica charantia in protecting the membrane integrity of liver cells has been demonstrated by its ability to inhibit the alcohol-mediated lipid peroxidation process in the liver (illustrated by the author).

The use of antioxidants has been shown to inhibit the progression of liver disease and improve the effectiveness of current therapies by reducing oxidative stress. Antioxidants may promote the dissociation of nuclear factor erythroid 2–related factor 2 (Nrf2) from the complex by altering the phosphorylation of Kelch-like ECH-associated protein-1 (Keap1) or Nrf2, leading to Nrf2 activation. Activation of Nrf2 results in its translocation to the nucleus, where it interacts with the antioxidant response element. This process results in increased expression of genes encoding antioxidant enzymes and phase II detoxifying enzymes, which are essential for cellular protection and recovery. Moreover, several studies have shown that certain antioxidants or plant extracts rich in antioxidants protect against hepatotoxin-induced liver injury by enhancing Nrf2 activation.[52] The oxidative mechanism is illustrated in Figure 3.

Figure 3.

Figure 3

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Nrf2-related antioxidant mechanisms (original creations).

Under unstressed conditions, the protein Keap1 represses Nrf2. However, in the presence of oxidative stress, Nrf2 is released from repression, thereby activating antioxidant genes and strengthening cellular defense mechanisms. In a study examining the hepatoprotective effects of M. charantia on NAFLD, serum concentrations of C-reactive protein and interleukin-6 were significantly reduced following supplementation (p<0.05). Similarly, sterol regulatory element-binding protein 1 (SREBP-1), a principal regulator of lipogenesis and a potential contributor to the development of fatty liver, was reduced following M. charantia supplementation, accompanied by decreased expression of fatty acid synthase (FAS) and acetyl-CoA carboxylase 1 (ACC-1) proteins, as well as reduced cholesterol and triglyceride (TG) concentrations. Inflammatory processes have been shown to induce the production of tumor necrosis factor-alpha (TNF-α), which may stimulate the maturation of SREBP-1 and contribute to lipid accumulation in hepatocytes. Therefore, it can be suggested that the effects of M. charantia on SREBP-1 and its target genes may help reduce inflammation. These findings indicate that M. charantia may serve as a promising agent for the prevention and treatment of NAFLD.[40]

The hepatoprotective properties of a formulation containing Ferula asafoetida, M. charantia, and Nardostachys jatamansi were examined in carbon tetrachloride-induced injury in rats. Enzymes including glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, and alkaline phosphatases were selected as markers for the investigation. A statistically significant decrease was observed in the levels of these enzymes (p<0.01).[53]

The acute toxicity of M. charantia fruits was investigated, and the median lethal dose (LD50) value was calculated to be >5000 mg/kg. Consequently, the fruit is considered relatively safe.[54] Nevertheless, research indicates that bitter melon may potentially interact with hypoglycemic drugs.[55] Furthermore, because M. charantia exhibits cytochrome P450 3A4 (CYP3A4) activity, there is a possibility of interaction with drugs metabolized by this enzyme.[56,57] The most frequently observed adverse effects are hypoglycemia and headaches.[55] Its use is not recommended during pregnancy and lactation. Studies in rats demonstrated the occurrence of cardiac hypertrophy in embryos, although no instances of lethality were observed.[58] Therefore, formulations containing M. charantia may potentially have adverse effects on the developing fetus.

Bioavailability

Bioavailability is one of the major challenges associated with herbal products.[59] It is important to investigate advanced technologies, such as nanoparticles and phytosomes, for bitter melon. Owing to the unpleasant flavor and limited bioavailability of M. charantia, innovative technologies such as nanoparticles and phytosomes may be utilized to enhance stability and bioavailability.[60] Studies involving nanoparticles have shown that herbal extracts may reduce toxicity while increasing activity.[61] The antibacterial efficacy of silver nanoparticles synthesized from M. charantia extract has been examined. The nanoparticle-treated group exhibited a notable increase in activity (p<0.005).[62] A study using the Huh-7 liver cancer cell line showed that M. charantia copper-iron nanoparticles promoted apoptosis. The IC50 was determined to be 324 μg/mL, indicating potential effectiveness.[63] Because nanoparticles are extremely small, they may also pose potential safety risks. Nanoparticle safety is a controversial subject due to the lack of evidence regarding both acute and chronic toxicity.[64]

Conclusion

Bitter melon (M. charantia) has a long history of use in traditional medicine spanning several centuries. Because the liver performs numerous essential functions in the body, maintaining liver health is of critical importance. Various pathways may contribute to the development of liver disorders; therefore, herbal compounds and extracts that act through multiple mechanisms play an important role. Studies investigating the hepatoprotective effects of M. charantia are summarized in Table 2. However, the lack of clinical trials and safety data represents a significant obstacle to the development of M. charantia as a therapeutic agent. Its traditional medicinal use provides valuable insight for modern drug development, particularly in elucidating its chemical constituents and determining their mechanisms of action through scientific investigation. M. charantia may be used in combination with other herbs, such as milk thistle, and compounds beneficial for liver health, such as curcumin and silymarin. Future studies may investigate potential synergistic effects between these agents. This review aimed to evaluate the hepatoprotective potential of M. charantia. However, the current state of clinical research and formulation development is insufficient in several aspects. Moreover, another major limitation is the lack of clinical studies investigating the optimal dosage and duration required to achieve hepatoprotective effects.

Table 2.

In vivo studies investigating the hepatoprotective effects of Momordica charantia L.

Plant part—solvent used Research model Dosage Results
Leaves—water[26] CCl4-induced hepatotoxicity in rats 200 mg/kg and 400 mg/kg ALT, AST, and ALP ↓ (p<0.05) SOD and CAT ↑ (p<0.05)
Leaves—50% ethanol[27] CCl4-induced hepatotoxicity in rats 100 mg/kg and 200 mg/kg ALT, AST ↓ (p<0.05); histopathological findings showed minimal cellular damage after treatment
Leaves—70% ethanol[28] CCl4-induced hepatotoxicity in rats 100 mg/kg and 200 mg/kg SGOT, SGPT, ALP, and total bilirubin levels improved (p<0.05)
Juice[29] Acetaminophen-induced liver injury in rabbits 5 mL/kg ALT, AST, and ALP ↓ (p<0.05)
Fruit—95% ethanol[30] Ammonium chloride-induced liver injury in rats 300 mg/kg AST, ALT, and ALP ↓ (p<0.05); decreased blood ammonia and plasma urea levels
Fruit—80% ethanol[31] Alcohol-induced hepatotoxicity in rats 25, 50, and 100 mg/kg SOD, GSH, and CAT ↑ (p<0.05)
Fruit—water[14] Restraint-stressed mice 250, 500, and 750 mg/kg Histopathological findings indicated intact liver cell structure and clearly defined hepatic cords; ALT and AST ↓ (p<0.05)
Fruit—Hexane[32] Rat model of hepatic ischemia-reperfusion injury 200 mg/kg Prevented increases in SGOT, SGPT, ALP, LDH, and CRP levels (p<0.01); prevented increase in MDA levels (p<0.05)
Leaves—70% methanol[33] Cadmium-induced hepatotoxicity in rats 300 mg/kg Cadmium caused fibrosis around the portal vein and disintegration of hepatocyte nuclei; pretreatment with extracts revealed prominent Kupffer cells
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ALP: Alkaline phosphatase; AST: Aspartate aminotransferase; ALT: Alanine aminotransferase; SGOT: Glutamate oxaloacetate transaminase; SGPT: Glutamate pyruvate transaminase; SOD: Superoxide dismutase; CAT: Catalase; GSH: Glutathione; LDH: Lactate dehydrogenase; CRP: C-reactive protein; MDA: Malondialdehyde.

Footnotes

How to cite this article: Altintas Gunduz D, Balaban Y, Koca Caliskan U. A traditional herbal remedy in liver diseases: Momordica charantia L. (kudret narı/bitter melon). Hepatology Forum 2026; 7(2):154–162.

Conflict of Interest

The authors have no conflict of interest to declare.

Financial Disclosure

The authors declared that this study has received no financial support.

Use of AI for Writing Assistance

The study did not use artificial intelligence (AI)-supported technologies (such as Large Language Models [LLMs], chatbots or image generators, ChatGPT).

Author Contributions

Concept: DAG, YB, UKC; Design: DAG, YB, UKC; Supervision: DAG, YB, UKC; Funding: DAG, YB, UKC; Materials: DAG, YB, UKC; Data Collection and/or Processing: DAG, YB, UKC; Analysis and/or Interpretation: DAG, YB, UKC; Literature Search: DAG, YB, UKC; Writing: DAG, YB, UKC; Critical Reviews: DAG, YB, UKC.

Peer-review

Externally peer-reviewed.

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