Int J Curr Pharm Res, Vol 17, Issue 5, 42-45Review Article

HEPATOPROTECTIVE HERBS: AN UPDATED REVIEW

KUNAL WALIA*, AJEET PAL SINGH, AMAR PAL SINGH

Department of Pharmacology, St. Soldier Institute of Pharmacy, Lidhran Campus, Behind NIT (R. E. C.), Jalandhar–Amritsar by pass, NH-1, Jalandhar-144011, Punjab, India
*Corresponding author: Kunal Walia; *Email: kunalwalia2000.k@gmail.com

Received: 10 Jun 2025, Revised and Accepted: 02 Aug 2025

ABSTRACT

Liver diseases are becoming a serious global health problem and may be caused by many toxic substances, including chemotherapeutic drugs, thioacetamide, carbon tetrachloride, certain antibiotics, excessive alcohol consumption, and microbes. Therefore, having a healthy liver is vitally important for good health and well-being. The liver is an important organ, contributing to the metabolism of the body and that of xenobiotics. There are many toxic substances which could cause liver damage (certain antibiotics, chemotherapeutic drugs, carbon tetrachloride, thioacetamide, and microbes, are mostly responsible for liver cell damage). The synthetic drugs that are available at this point to deal with liver dysfunction causes additional harm to the liver. Hence, the use of herbal medicines has grown and become popular. The important medicinal herbs that can be used to treat liver diseases with the least impact on the kidneys have been described. Because of the hepatoprotective character, antioxidant-related characteristics and least harm to kidneys, features of the newly described medicinal plants can be used to develop new medicines for the prevention and treatment of liver diseases.

Keywords: Herbal drugs, Hepatotoxicity, Liver diseases, Medicinal plant, Factors

© 2025 The Authors. Published by Innovare Academic Sciences Pvt Ltd. This is an open access article under the CC BY license (https://creativecommons.org/licenses/by/4.0/)
DOI: https://dx.doi.org/10.22159/ijcpr.2025v17i5.7045 Journal homepage: https://innovareacademics.in/journals/index.php/ijcpr

INTRODUCTION

With an average adult weight of 1.4 kg, the liver is the heaviest gland in the human body (after the skin) and the second largest organ. It occupies the majority of the right hypchondiac and a portion of the epigastric regions of the abdominopelvic cavity and is located inferior to the diaphragm [1]. The liver plays a major role in the metabolism and excretion of drugs. Detoxicfying pharmaceuticals and xenobiotics in the liver via drug metabolizing enzymes (DMEs) is one of the significant processes involved in the restoration of homeostasis [2]. The liver accounts for 2 % to 3 % of normal body weight. It normally has four lobes, each defined in both morphological and functional annatomy. It is located underneath the right hemidiaphragm (right upper quadrant of the abdominal cavity) and has ligamentous attachments to the area. It is protected by the ribcage and is held in place by peritoneal reflections. Although the liver's ligamentous attachments are not true ligaments, they are avascular and continuous with the Glisson capsule or the liver's visceral peritoneum [3]. Hepatotoxicity refers to damage to the liver caused by chemicals. Drug-induced damage to the liver can cause acute and chronic liver disease. The liver is susceptible to the toxicity wrought by many other chemicals, and the liver's role to metabolize and excrete toxins is of paramount importance. Several drugs, including acetaminophen, can lead to harm to an organ by overtaking otherwise modest therapeutic dosages. The liver can also be damaged by other chemical agents, e. g., in factories or laboratories, naturally occurring compounds (e. g., microcystins), and herbal medicines. Substances that are harmful to the liver are also termed hepatotoxins [4]. The most common reason for drugs to be withdrawn from the market is liver damage; drug-induced liver damage has been linked to 900+drugs, and hepatotoxicity and drug-induced liver injury are also responsible for the failure of many compounds that are under investigation so that it is essential that new drug screening assays could use new stem cell-derived hepatocyte-like cells, which will determine hepatotoxicity much earlier in the drug developmental process. Subclinical liver damage occurs with the administration of chemicals and will typically only manifest as abnormal liver enzymes. Drug-induced liver damage is responsible for 50% of all cases of acute liver failures and 5% of all hospital admissions [5]. Most of these substances are absorbed through the gastrointestinal tract, but a smaller number though parenterally or absorbed through the skin or lungs immediately (inhalants). The majority of drugs and xenobiotics are lipophilic because they pass readily through the intestine and hepatocyte cell membranes. Metabolism in the hepatocyte alters drug structure in such a way that the drug is more hydrophilic, producing water soluble metabolites which are cleared in urine or bile. Drug metabolic pathways are divided into phase I pathways (oxidation, reduction, hydrolysis) mediated by various cytochrome P450 isozymes and phase II conjugation pathways (glucuronidation, acetylation, sulphation, methylation) mediated by various transferases. Highly polar drugs do not require metabolism. Some drugs may degrade spontaneously [6].

Genetic and nongenetic risk factors

Risk factors for susceptibility to drug-induced hepatotoxicity

Table 1: Therapeutic agents causing hepatotoxicity [7, 8]

Antimicrobial Analgesics and anti-tuberculosis drug Immunomodulator Antiepileptics
Amoxicillin NSAIDs Interferon-beta Phenytoin
Isoniazid Rifampicin, Rifabutin Interferon-alpha Lamotrigine
Sulfamethoxazole Pyrazinamide Anti-TNF agents Azathioprine Valproic Acid
Trimethoprim Prothionamide Cyclophosphamide Carbamazepine

Table 2: Medicinal plants with hepatoprotective potentials

Name of the plant Extract used Hepatotoxicity-inducing agents Biochemical and histopathological parameter studied Hepatotoxicity-inducing agents
Phyllanthus Muellarianus (leaves) [9] Aqueous ALP, ALT, AST, ALB, TB, CAT Acetaminophen 400 mg/kg
Picrorhizakurroa (Roots) [10] Ethanol SGOT, SGPT, ALP CCl4 2.60 ml/kg
Bauhinia Variegate (Stem barks) [11] Alcohol AST, ALP, GGT, ALT CCl4 100 and 200 mg/kg
Galium aparine (whole) [12] Alcohol ALT, AST, and ALP CCl4 2 ml/kg
Ficus cordata (roots) [13] Methanol/ethyl LDH CCl4 400 mg/kg
Canna indica (Aerial parts) [14] Methanol SGPT, SGOT, TB, CAT, GSH, LPO CCl4 100 and 200 mg/kg
Curcuma longa (Rhizome)[15] Ethanol ALT, ALP, and AST PCM 600 mg/kg
Dodonaeaviscosa (leaves) [16] Methanol AST, LDLC, ALT Alloxan 500 mg/kg
Ecliptaprostrate (Fresh leaves)[17] Methanol ALT, AST, and serum bilirubin CCl4 10 80 mg/kg
Boerhaviadiffusa (Roots)[18] Ethanol SGPT, SAP, TGs, and total lipid levels Country‑made liquor 200 and 400 mg/kg
Tylophora (leaves) [19] Methanol SGPT, ALP, SGOT CCl4 200 and 300 mg/kg
Tylophora (Leaves) [20] Methanol SGPT, ALP, SGOT CCl4 200 and 300 mg/kg
Tridax Procumbens (Aerial parts) [21] Ethanol AST, LDH, ALT, ALP, GGT, TB d‑GalN/lPS 300 mg/kg
Opuntia ficus‑indica (Leaves) [22] Aqueous AST, ALT, Creatinine, Urea, Uric acid CCl4 2, ml/kg
Apium graveolens (Seeds) [23] Methanol SGOT, SGPT, SALP CCl4 250 mg/Kg
Opuntia ficus‑indica (Stem) [24] Aqueous ALAT, ASAT, ALP, LDH, CHL CPF 1500 mg/kg
Agrimoniaeupatoria (Aerial part) [25] Aqueous AST and ALT Ethanol 100 and 300 mg/kg
Vitis vinifera (Leaves) [26] Alcohol AST and ALT CCl4 125 mg/kg
Rheum palmatum (Aerial part) [27] N/A N/A CCl4/ethanol 25 and 100 mg/kg
Ziziphus oenoplia (Roots) [28] Alcohol SGOT, SGPT, SALP, SB, SOD, CAT, GST INH and RIF 150 and 300 mg/kg
Corylus avellana (Leaves) [29] Aqueous GPT and GOT CCl4 and acetaminophen NA
Cinnamomum Cassia (Bark) [30] Ethanol TP, albumin, TB, direct bilirubin, Dimethyl nitrosamine 40 mg/kg
Pistacia lentiscus (Gums) [31] NA AST, ALT and MDA, GSH, GPx, GST, GR, SOD CCl4 NA
Punica granatum (Edible and Portion) [32] Acetone AST, ALT, and LDH INH and RIF 400 mg/kg
Rosa damascene Mill (Flower) [33] Aqueous AST, ALT, ALP, LDH, ALBTB, urea and creatinine Acetaminophen 250, 500 and 1000 mg/kg
Cucurbita maxima (Aerial parts) [34] Methanol SGPT, SGOT, ALP, TP, and TB CCl4 250 and 500 mg/kg
Cynara (Root) [35] Hydroalcohol ALT, ALP, AST, CCl4 900 mg/kg
Taraxacum Officinale (Roots) [36]

Hydroalcoholic

acid

 TBARS, GST, GSH, SOD, CAT, GR, and Ethanol 250 mg/kg
Tragopogon Porrifolius (Edible root and shoot) [37] Methanol CAT, SOD and GSTAST, ALT CCl4 250 mg/kg
Baliospermum Montanum (Root) [38] Methanol GOT, GPT, ALP, TB, TC, TB TAA 2000 mg/kg
Tephrosia Purpurea (Aerial parts) [39] Ethanol AST, GSH, ALT, ALP, TB, GGT TAA 500 mg/kg
Alchornea Cordifolia (leaves) [40] Methanol SGOT/AST, SGPT/ALT, ALP CCl4 300 mg/kg
Glycosmis pentaphylla Corr. (Leaves, bark) [41] Methanol ALT/SGPT, AST/SGOT, CHL CCl4 500 mg/kg
Wedelia chinensis L. (Leaves) [42] Ethanol AST, ALT, ALP, Protein CCl4 200 mg/kg
Cassia fistula (Seeds) [43] Methanol SGOT, SGPT, ALP, and bilirubin PCM 200 and 400 mg/kg
Tylophora (Leaves) [19] Methanol SGPT, ALP, SGOT CCl4 200 and

CONCLUSION

New hepatoprotective drugs need to be discovered because current medications that treat liver diseases, particularly a viral hepatitis or any degree of chronic liver disease, do not serve the unmet needs of the patients and may have detrimental renal effects. Because liver function is of upmost importance to the human body, liver disease and liver injury is now ranked as one of the most impotent health issues in the world. The causes of liver injury primarily include excessive intake of alcoholic beverages, lack of dietary discipline, herbal supplement use, viral, bacterial and parasitic infections, autoimmune diseases, neoplastic processes, metabolic disorders, and substance abuse. For example 50% of people living in developing countries that have liver disease or any form of liver disease choose to use herbal medicine for treatment and therefore have tapped worldwide interest. The majority of herbal extracts that are available today have demonstrated great effect with mild effects on regulating the signs and symptoms associated with liver disease or liver injury. In the treatment of liver disease or the symptoms associated with liver disease, the herbs may have provided a new avenue to explore in the constrained options for medicinal measures.

ACKNOWLEDGMENT

It’s our privilege to express the profound sense of gratitude and cordial thanks to our respected chairman Mr. Anil Chopra and Vice Chairperson, Ms. Sangeeta Chopra, St. Soldier Educational Society, Jalandhar for providing the necessary facilities to complete this review work.

FUNDING

Nil

AUTHORS CONTRIBUTIONS

All authors have contributed equally

CONFLICT OF INTERESTS

Declared none

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