PRESENT SCENARIO OF HEPATOPROTECTIVE POTENTIAL OF MEDICINAL PLANTS: AN UPDATED REVIEWHTML Full Text
PRESENT SCENARIO OF HEPATOPROTECTIVE POTENTIAL OF MEDICINAL PLANTS: AN UPDATED REVIEW
Payal Saiju *, Priya Jain and D. P. Chatterjee
Faculty of Pharmacy, SAGE University, Bypass Road, Kailod Kartal, Indore - 452020, Madhya Pradesh, India.
ABSTRACT: The liver is the principal site for metabolism and excretion in the body. The human liver metabolizes substances by various biochemical pathways, including oxidation, reduction, hydration, condensation, hydrolysis, conjugation or isomerization. Disorder of any of therefore mentioned process may lead to liver cell injury, what we call as hepatotoxicity, which in turn leads to many diseases. Such diseases are responsible for higher mortality rates worldwide. Hepatotoxicity can be due to medicines, chemicals, dietary disturbances, or herb induced liver damage via hepatotoxins. A number of herbal and herbomineral preparations are available in the Ayurveda, the traditional Indian medicine, which has been investigated for their hepatoprotective potential to treat different types of liver disorders. The use of natural elements to eliminate the root cause of the disease by restoring balance at the same time creates a healthy lifestyle to prevent the recurrence of imbalance. Herbal medicines have existed worldwide with long recorded history, and they were used in ancient Chinese, Greek, Egyptian, and Indian medicine for various therapies purposes. World Health Organization estimated that 80% of the word's inhabitants still rely mainly on traditional medicines for their health care. The subcontinent of India is well-known to be one of the major biodiversity centers with about 45,000 plant species. The present review is focused on different herbal plants that have the potential to cure the hepatotoxicity.
Hepatoprotective, Herbal, Hepatotoxicity, Liver, Ayurveda
INTRODUCTION: The liver is the second largest (after the skin) organ in the human body and the largest gland (weighing an average of 1500 g). The liver is located in the upper right-hand portion of the abdominal cavity, beneath the diaphragm, and on top of the stomach, right kidney, and intestines. Shaped like a cone, the liver is a dark reddish-brown organ that weighs about 3 pounds.
The liver is an organ only found in vertebrates which detoxifies various metabolites, synthesizes proteins, and produces biochemicals necessary for digestion 1, 2.
The liver is the most important organ that plays an important role in maintaining various physiological processes in the body. Liver damage is very common because the liver is a key organ in the detoxification process. Hepatotoxic chemicals damage liver cells primarily by producing ROS, some of which form covalent bonds with the lipid tissue. Due to excessive exposure to hazardous chemicals, sometimes the free radicals generated are so high that they overpower the natural defense system, leading to hepatic damage 3.
Hepatitis, a common disorder of varying severity, can lead to cirrhosis, liver failure, and death. If acute liver disorders are not promptly treated, the damage will go to chronic forms characterized by continuing hepatocellular necrosis and inflam-mation, usually with fibrosis, which tends to progress to cirrhosis and liver failure 4.
There are five main viruses, referred to as types A, B, C, D, and E. These five types are of the greatest concern because of the burden of illness and death. Liver injury or liver dysfunction is a major health problem that challenges not only health care professionals but also the drug regulatory agencies and the pharmaceutical industry. Despite enormous advances in modern medicine, there are no completely effective drugs that stimulate hepatic function, that offer complete protection of the organ, or that help to regenerate hepatic cells 5. The aim of these alternatives being more effective and less toxic.
Herbal medicines have been used in the treatment of liver disease for a long time. In this context, therapeutic alternatives are limited. For this reason, there is a great need to find new drugs for the treatment of these pathologies.
There are potent indigenous herbal medicines available for the treatment of liver disorders in various parts of the world, and most of them have not yet been scientifically validated. If they are conducted, it could lead to the development of cost-effective drug. In the absence of a reliable liver protective drug in the modern system of medicine, a number of medicinal preparations in Ayurveda are recommended for the treatment of liver disorders. Natural remedies from medicinal plants are considered to be an effective and safe alternative treatment for liver diseases 6.
The plant-derived phytoconstituents (polysaccha-rides, proteins, and flavanoids, lignans, carotenoids, etc.) stimulate the immune system and maintaining hepatic diseases 7. Flavonoids are phenolic compounds widely distributed in plants and have been reported to exert multiple biological effects, including antioxidant and free radical scavenging abilities 8. There are a number of hepatoprotective herbs that have been reported. The present review is aimed at compiling data on promising phytochemicals from hepatoprotective herbs.
Hepatotoxicity Inducing Agents: Many xenobiotics like chemicals, drugs, household things, herbs and environmental factors are well-known to induce hepatotoxicity. Most significant for xenobiotic-induced liver injury, the centri-lobular (zone-3) hepatocytes are the 1st sites of hemoprotein P450 accelerator activity, which regularly makes them at maximum risk of xenobiotic-induced liver injury. CCl4, N-nitrosodiethylamine, Acetylaminofluorene, Gala-ctosamine, d-Galactosamine/Lipopolysaccharide, TAA, Antitubercular drugs, PCM, Arsenic etc. have been shown to induce experimental hepato-toxicity in laboratory animals 9.
FIG. 1: ANATOMY OF LIVER
Model of Hepatotoxicity:
Thioacetamide Induced Hepatotoxicity Model: TAA, originally used as an antimycotic agent, is potent toxin bioactivated by hemoprotein P450 to sulfine (sulfoxide) and sulfene (sulfone) metabolites; it is known to induce liver cirrhosis of the liver in murine models that is caused by free radical-mediated super-molecule peroxidation. TAA administration results in liver harm in experimental rats by a marked increase alanine aminotransferase (ALT), aspartate aminotransferase (AST) in serum and malondialdehyde in the liver, conjointly centrilobular necrosis in internal organ design. TAA interferes with the movement of RNA from the nucleus to the protoplasm, which can cause membrane injury. A substance of TAA is chargeable for internal organ injury. TAA cut back the number of viable hepatocytes, likewise as rate oxygen consumption. Usually, TAA dosage is 100 - 300 mg/kg, administrated subcutaneous or intra-peritoneal. Future administration and/or high doses of TAA ends up in an organic chemistry modification, microscopic anatomy, and characteristic lesion in rat liver, which corresponds to cirrhosis of the liver-like patterns of micro-nodular liver cirrhosis in humans and associated protein-energy deficiency disease. Investigation on therapeutic principles ought to be done throughout TAA administration (prophylactic agents) or inside 2 months when the withdrawal of harmful agents (therapeutics) 10, 11.
Carbon Tetrachloride Induced Hepatotoxicity Model: CCl4 is a strong hepatotoxin producing hepatic necrosis. Liver injury due to CCl4 in experimental rats has been induced experimentally by many investigators. CCl4 is metabolized by cytochrome P450 in endoplasmic reticulum and mitochondria with the formation of highly reactive trichloromethylperoxy free radicals, which initiate lipid peroxidation and finally cell necrosis. Administration of a single dose of CCl4 to a rat produces, within 24 h, centrilobular necrosis and fatty changes. The development of necrosis is associated with the leakage of hepatic enzymes into serum. The toxic dose of CCl4 is 0.1 - 3 ml/kg administrated intraperitoneally12.
Paracetamol Induced Hepatotoxicity Model: PCM, a widely used analgesic and antipyretic drug, produces acute liver damage in high doses. PCM administration causes necrosis of the centrilobular hepatocytes characterized by nuclear pyknosis and eosinophilic cytoplasm followed by the large excessive hepatic lesion. The covalent binding of N-acetyl-P benzoquinoneimine, an oxidative product of PCM to sulphydryl groups of protein, result in degradation and lipid peroxidation of glutathione level and thereby, produces cell necrosis in the liver. The dose of PCM is 1 - 2 gm/kg administrated orally 13.
Chloroform Induced Hepatotoxicity Model: Chloroform has toxic effects similar to those of CCl4. Metabolism by microsomal cytochrome P450 is obligatory for the chloroform induced hepatic, renal, and nasal toxicity. It seems that the cytochrome P450-mediated oxidative metabolism of chloroform results in the formation of inorganic chloride (excreted in the urine), carbon dioxide (exhaled), phosgene, and some hepatic covalently bound carbon (either via free radical or phosgene formation). Extensive covalent binding to the kidney and liver protein has been found in direct relationship with the extent of hepatic centrilobular and renal proximal tubular necrosis 14.
Rifampicin Induced Hepatotoxicity Model: Patients on coincidental rifampicin medical care have associate accumulated incidence of liver disease. This has been postulated due to rifampicin-induced cytochrome P450 enzyme-induction, inflicting associate accumulated production of the toxic metabolites from acetyl hydrazine (AcHz). Rifampicin conjointly will increase the metabolism of isoniazid to isonicotinic acid and reducer, each of that is hepatotoxic. The plasma half-life of AcHz (a metabolite of isoniazid) is shortened by rifampicin, and AcHz is quickly reborn to its active metabolites by increasing the oxidative elimination rate of AcHz, which is said to the upper incidence of liver necrosis caused by isoniazid and rifampicin together. Rifampicin conjointly interacts with antiretroviral medicine and affects the plasma levels of those drugs also as the risk of hepatotoxicity 15.
Isoniazid Induced Hepatotoxicity Model: Isoniazid hepatotoxicity may be a common complication of antituberculosis medical care that ranges in severity from well elevation of serum transaminases to hepatic failure requiring liver transplantation. This can be not caused by high plasma bactericide levels; however, it seems to represent an individual response. Isoniazid is metabolized to mono AcHz, which is additional metabolized to a toxicant product by haemoprotein P450 resulting in hepatotoxicity. Human genetic studies have shown that haemoprotein P4502E1 (CYP2E1) is concerned with antitubercular drug hepatotoxicity. The CYP2E1/c1 genotype is related to a better CYP2E1 activity and will result in a better production of hepatotoxins. Experimental Rodent studies showed that Isoniazid and Hydrazine induce CYP2E1 activity. Isoniazid has an inhibiting result on CYP1A2, 2A6, 2C19, and 3A4 activity. CYP1A2 is usually recommended to be concerned with reductant detoxification. Isoniazid will induce its own toxicity, presumably by the induction or inhibition of those enzymes 16.
Other Drugs Induced Hepatotoxicity Model: Few other drugs reported to cause hepatotoxicity are Glucocorticoids, Antibiotics (Amoxicillin, Ciprofloxacin, Erythromycin), Oral contraceptives and antifungals (Fluconazole, itraconazole) 17.
Drug Hepatotoxicity: A wide variety of chemicals produces clinical and pathological hepatic injury. Biochemical markers (e.g., alanine transferase, alkaline phosphatase, and bilirubin) are often used to indicate liver damage. Liver injury is defined as a rise in either
- ALT level more than three times of upper limit of normal (ULN),
- ALP level more than twice ULN, or
- Total bilirubin level more than twice ULN when associated with increased ALT or ALP18, 19.
Mechanism of Liver Damage: The possible mechanisms of liver toxicity are due to excessive use of drugs and other xenobiotics in the context of hepatic physiology, metabolism, and cell biology. The important liver injury mechanisms can be a consequence of metabolism and/or direct cell toxicity of chemicals. These mechanisms include bile acid-induced liver cell injury during cholestasis, pathophysiological effects of mitochondrial dysfunction, and cell damage by reactive oxygen and nitrogen species. Theses is the importance of vascular (Kupffer cells, neutrophils) and intracellular generation of reactive oxygen by mitochondria and xenobiotic inducible enzymes (e.g., CYP 4502E1) 20 Table 1.
TABLE 1: AN UPDATED REVIEW ON HEPATOPROTECTIVE POTENTIAL OF MEDICINAL PLANTS
|Hepatoprotective activity/study outcomes|
|1||Abutilon indicum 21||Whole
zoic acid, Caffeic acid
|Activates antioxidative enzyme against CCl3 (Inducer)|
|2||Adhatodavasica 22||Leaves||Aqueous||Vasicine, vasicol, vasicinone,
peganine, adhatodine, vasicolinone
|Reduces elevated levels of SGOT and SGPT|
|3||Aloe barbadensis 23||Aerial parts||Pet. ether, CHCl3,
|Barbaloin, chrysophanol, glycoside aloe‑emodin, glucose, galactose, mannose and galacturonic acid
|Protects against increased lipid peroxidation and maintained glutathione contents by antioxidant property|
|4||Amaranthus spinosus 24||Whole
|Ethanol||Flavonoids, phenolic, steroids, terpenoids, lipids, saponins||Normalises serum biochemical parameter by antioxidant activity|
|5||Anogeissus latifolia 25||Bark||Hydroalcoholic||Tannins, gallic acid, ellagic
acid, lutin and quercetin
|Reduces the ALT, AST, ALP levels and lipid peroxidation|
|6||Apium graveolens 26
|Seeds||Methanol, Pet. Ether, Acetone||Flavanoids, anthrons,
|Reduces the elevated serum transaminases, ALP, total protein and albumin|
|7||Aspalathus linearis 27||Leaves||Aqueous||Flavanoids||Antifibrotic effect, anticirrhotic effect|
|8||Asteracantha longifolia 28||Seeds||Methanol||Lupeol and stigmatsterol||Reduces serum phospholipid level|
|9||Azadirachta indica 29
|Leaves||Ethanol||Quercetin, rutin||Balances serum biochemical levels by antioxidant activity|
|10||Arachniodes exilis 30
|Rhizome||Ethanol||Polyphenols||Reduces the levels of SGPT and SGOT|
|11||Artemisia absinthium 31||Stem,
|Flavonoid glycosides||Facilitates to maintain intracellular antioxidant levels|
|12||Alchornea cordifolia 32
|Leaf||Methanol||Saponins, tannins and flavonoids||Inhibits the elevated serum levels of ALT and total bilirubin|
|13||Annona senegalensis 33||Root||Methanol||Steroids, flavonoids, terpenoids||Decreases the ALT and AST value|
|14||Andrographis paniculata 34||leaves||Aqueous||Diterpenoids, andrographolide, flavones||Decreases the level of serum AST,ALT, LDH, ALP and total bilirubin|
|15||Boerhaavia diffusa 35||Leaf||Aqueous, ethanol||Phenolic content, flavonoid content, vitamin C, vitamin E||Preserves antioxidant potential|
|16||Butea monosperma 36||Flowers||Aqueous||Butein, butin, isobutrin,
|Prevents from oxidative potential by inducers|
|17||Byrsocarpus coccineus 37
|Leaf||Aqueous||Flavonoids and alkaloids||Rich in antioxidants and strongly inhibit lipid peroxidation|
|18||Bupleurum chinense 38
|Root||Hot water||Flavonoids and polysaccharides||Reduces the AST, ALT, ALP, LDH and increases the GSH, GR, GST and SOD|
|19||Calotropis procera 39||Flowers||Hydroethanol||quercetin‑3‑rutinoside, flavonoids||Prevents the depletion of GSH levels|
|20||Cassia fistula 40||Leaves||n‑hexane||Phenolic compounds, cyaniding B2, biflavonoids, triflavonoids||Facilitates in lowering the serum transaminases, bilirubin and ALP|
|21||Cistanche tubulosa 41||Fresh
|Methanol||Kankanosides H1, H2 and I,
|Reduces TNF‑alpha‑induced cytotoxicity in liver cells|
|Leaf||Pet. ether||Phytosterols, phenolic
|Decreases hepatocyte peroxidation
and lipoprotein lipase in liver
|23||Carya illinoensis 43||Nut shells||Aqueous||Polyphenols, condensed tannins||Inhibits Fe2+ induced lipid peroxides|
|24||Cyathea gigantean 44||Leaves||Methanol||Triterpenes, sterols,
saponins and flavonoids
|Reduces the elevated level of SGOT, SGPT, ALP and TB|
|25||Crataeva nurvala 45
|Stem bark||Ethyl acetate||Lupeol, lupeollinoleate||Scavenges peroxyl radicals by bolstering the levels of antioxidant enzyme system|
|26||Decalepis hamiltonii 46||Root||Aqueous||Flavonoids||Inhibits lipid peroxidation|
|27||Daucus carota 47||Seeds||Methanol||Flavonoids||Decreases SGOT, SGPT and ALP|
|28||Emblica officinalis 48||Fruit||Hydro-alcohol||Tannins, Flavonoids, Saponins, Alkaloids, Phenol||Reverses serum enzyme activity i.e., AST, ALT, ALP and bilirubin|
|29||Enicostemma axillare 49||Whole
|Ethyl acetate||Secoiridoid glycoside||Decreases the lipid peroxidation|
|30||Euphorbia fusiformis 50
|Tubers||Ethanol||Ellagic acid||Possesses antioxidative
|31||Fumaria indica 51||Whole
bicuculine, and fumariline
|Reduces the elevated levels of serum transaminases (SGOT, SGPT)|
|32||Fumaria species 52||Whole
|Ethanol||Total phenol and flavonoid||Decreases plasma or hepatic MDA|
|33||Fumaria indica 53||Whole
|Reduces the serum biochemical indicators (AST, ALT, ALP and LDH)|
|34||Ginkgo biloba 54
|Leaves||Pet. ether||Polyprenols||Reduces the elevated level of MDA by possessing zthe antioxidant ability|
|Gallic acid||Facilitates to maintain intracellular antioxidant levels|
|36||Gardenia gummifera 56
|Roots||Methanol||Flavonoids and phenols||Suppresses the elevated levels of serum AST, ALT, ALP, LDH and MAD|
|37||Glycyrrhiza glabra 57
|Roots||CCl4||18 β‑Glycyrrhetinic Acid||Reduces the elevated levels of LDH,GOT, GPT and MDA and increases
the reduced levels of SOD and GSH
|38||Gentiana olivieri 58
|Aerial parts||Ethyl acetate||Isoorientin||Decreases the MDA, transaminase levels in plasma and hepatic tissue|
|39||Halenia elliptica 59||Whole plant||Methanol||Carotenoids, gallic acid||Strong free radical scavenging activity|
|40||Heterotheca inuloides 60||Whole
|Acetone, Methanol||Quercetin, Stigmasterol,
|Inhibits lipid peroxidation|
|41||Hippophae rhamnoides 61||Leaves||Aqueous, Hexane,
|Gallic acid, myricetin, quercetin, kaempferol and isorhamnetin||Protects against hepatocytic necrosis, fatty changesand oxidative damage|
|Aqueous||Saponins, tannins, flavonoids, anthraquinones, terpenoids||Reduces lipid peroxidation and scavenges free radicals|
|43||Hibiscus esculentus 63||Dried pods||Ethanol||Flavonoids, tannins,
sterols and triterpenes
|Decreases elevated serum SGOT, SGPT, ALP, GGT, cholesterol and TG|
|44||Hibiscus vitifolius 64||Root||Methanol||Sterols, glycosides, triterpenoids, mucilage and flavonoids||Reduces the levels of serum AST, ALT, ALP, LDH levels|
|45||Litchi chinensis 65||Fruit||pulp Fruit juice||Vitamin C, phenolic contents||Anti lipid peroxidation, anti‑apoptosis|
|46||Luminetzera racemosa 66||Bark||Ethanol, Water||Flavonoids, alkaloid, polyphenol||Activates cytochrome‑P 450 enzyme system in the liver|
|47||Lycium chinense 67||Fruit||Ethyl acetate||Cerebrosides and
|Blocked the release of SGPT|
|48||Momordica dioica 68||Leaves||Aqueous||Flavonoids||Free radical‑ scavenging Property|
|49||Morus bombycis 69
|Aqueous||2, 5‑dihydroxy‑4, 3’‑di (β‑d‑glucOpyranosyloxy)‑trans‑stilbene||Antioxidant property|
|50||Melothria heterophylla 70||Aerial parts||Ethanol||β‑Sitosterol, glycosides,
saponin and flavonoids
|51||Murraya koeniggi 71||Leaf||Aqueous||Tannins and the
|Anti lipid peroxidative property|
|52||Moringa oleifera 72||Stem bark||Pet. ether, CCl4||Phenolic content and flavonoids||Antioxidant property|
|53||Murraya koenigii 73||Leaf||Hydro‑ethanol
|Flavonoids||Decreases the levels of AST, AST and ALP|
|54||Mallotus japonicas 74||Whole
|Bergenin||Prevents the elevation of MDA and glutathione content in the liver|
|55||Nymphae stellata 75||Flower||Hydro‑alcohol||Sesquiterpene lactones,
|Activates antioxidative enzymes and stabilizes hepatic membrane|
|56||Nicotiana glauca 76
|Leaves||Aqueous||Flavonoids and phenols||Reduces the ALP, ALT,AST and TB level|
|57||Phyllanthus amarus 77||Leaf||Ethanol||Flavonoids, phenols,
polyphenols and lignans,
|Enhances level of GSH, SOD, CAT and reduces GST, LPO level in the liver|
|58||Phyllanthus niruri 78
|Lignans, phyllanthin, flavonoids, Glycosides and tannins.||Inhibits membrane lipid peroxidation, scavenges DPPH radical|
|59||Piper chaba 79||Fruit||Aqueous acetone||Piperchabamides E, G, and H||Inhibits TNF‑alpha in liver|
|Methanol||Flavonoids||Decreases levels of serum enzymes (SGOT and SGPT)|
|61||Prunus armeniaca 81||Seed
|Ethanol||Flavonoids, vitamin‑C and carotenoids||Anti‑lipid zeroxidative and free radical scavenging|
|62||Pleurotus eryngii 82, 83||Dried fruits||Water||Polysaccharides, lipids, peptide, sterols, and dietary fibre
|Increases the activities of
antioxidant enzymes SOD, CAT,GSH and prevents excessive lipid formation in liver
|63||Pistacia lentiscus 84||Leaves||Aqueous||Flavonoids and phenols||Reduces ALP, ALT, AST and TB level|
|64||Phillyrea latifolia 85||Leaves||Aqueous||Flavonoids and phenols||Reduces ALP, ALT, AST and TB level|
|65||Rosa laevigata 86
Procaspase‑8, FasL in liver
|66||Spirulina platensis 87||Spirulina
α tocopherol, α‑‑lipoic acid
|Free radical scavenging properties and antioxidant activity|
|67||Terminalia catappa 88||Leaves||Chloroform||Flavonoids (Keampferol,
quercetin), tannins (punicalin, 4punicalagin, tercatin), saponins, phytosterols
|Prevents the mitochondrial disruption,
Intra mitochondrial Ca2+ overloadand suppresses Ca2+ ATPase activity
|68||Terminalia chebula 89
|Fruit||Ethanol||Chebuloside II||Antioxidant and act as membrane stabilizer|
|69||Thunbergia laurifolia 90||Leaves||Aqueous||Apigenin, casmosiin,
|Decreases ALT and AST release in liver|
|Ethanol||Saponin and punarnavine||Stimulates hepatic regeneration|
|Methanol||Phenolics and flavonoids||Reduces lipid peroxidation|
|72||Talinum triangulare 93||Whole
|Aqueous||Polysaccharides||Hydroxyl radical scavenging activity|
|73||Trichilia emetic 94||Root||Aqueous||Polyphenols, flavonoids
|Scavenges the reactive oxygen species|
|Polyphenolic||Polyphenolic compounds||Reduces LDH leakage and normalizes GSH/GSSG ratio|
|75||Tilia argentea 96
|Flowers||Methanolic||Flavonol glycoside||Inhibits SGPT, SGOT elevations and suppresses TNF‑α production|
|76||Viburnum tinus 97||Leaves||Aqueous,
|Flavonoids and biflavonoids||Antioxidative property, scavenges excessive nitrous oxide radicals|
|77||Vitex negundo 98||Leaf||Ethanol||Flavonoids, Vitamin C||Reduces oxidative stress|
|78||Vitex trifolia 99||Leaf||Aqueous and
|Persicogenin, artemetin, luteolin, penduletin and chrysosplenol‑D||Decreases the rise of serum enzymes and total protein level in liver|
|79||Vitis vinifera 100||Leaves||Ethanol||Halimane‑type diterpenes,
|Reduces MDA, AST, ALT and GSH levels of plasma and liver tissue|
|80||Woodfordia fruticosa 101||Flowers||Pet. ether,
|81||Zanthoxylum armatum 102||Bark||Ethanol||Isoquinoline alkaloid,
berberine, flavonoids and
|Increases the levels of antioxidant
enzymes: SOD and catalase
|82||Zosima absinthifolia 103||Roots||Pet. ether||‑deltoin and (+)‑columbianadin||Inhibits TNF alpha|
Pet. ether-Petroleum ether, CCl4‑Carbon tetrachloride, SGOT‑Serum glutamic oxaloacetic transaminase, SGPT‑Serum glutamate pyruvate transaminase, ALT‑Alanine transaminase, AST‑Aspartate aminotransferase, ALP‑Alkaline phosphatase, LDH‑Lactic acid dehydrogenase, GSH‑Glutathione Peroxidase, GR‑Glutathione reductase, GST‑Glutathione S‑Transferase, SOD‑Superoxide dismutases, TB‑Total bilirubin, MDH‑. Malate dehydrogenase, MDA‑Malondialdehyde, TG‑Triglyceraldehyde, CAT‑Catalase, LPO‑Lipid peroxidation, DPPH‑2,2‑diphenylpicrylhydrazyl
DISCUSSION: The goal of ethnopharmacological studies on medicinal plants should not be restricted to find new prototype pure compounds as drugs. Active extracts, fractions, or a mixture of fractions/extracts may prove very effective drugs. Plant drugs (combinations or individual drug) for liver diseases should possess sufficient efficacy to cure severe liver diseases caused by toxic chemicals, viruses (Hepatitis B, Hepatitis C, etc.), excess alcohol intake, etc. A single drug cannot be effective against all types of severe liver diseases. Effective formulations have to be developed using indigenous medicinal plants, with proper pharmacological experiments and clinical trials. The manufacture of plant products should be governed by standards of safety and efficacy.
CONCLUSION: From this review study, it is clear that the medicinal plants play a significant role against various diseases. Different medicinal herbs and plants extracts have potent hepato-protective activity in various animal models. The hepatoprotective activity is probably due to the presence of flavonoids, phenolic compounds, polyphenols, etc. in all few herbal plants. The results of this study indicate that extracts of leaves and plant extracts of some medicinal plants have good potentials for use in hepatic disease. The present review study gives evidential explore the mechanism of action of medicinal plants against experimentally induced hepatotoxicity.
The predicted mechanism of action of various plant extracts may be attributed to antioxidant properties and the presence of flavonoids, to increase the reduced level of blood glutathione in experimental animal models, to increase total proteins, to inhibit lipid peroxidation and increase in the antioxidant enzymatic activity, to decrease the hepatic marker enzymes (AST, ALT, ALP, and arginase) and total bilirubin in plasma, to enhance antioxidative enzymes, including SOD, GPx, CAT and GST, to decrease MDA level, SGOT, SGPT, etc. Hence, the review study is concluded that the herbal drug possesses hepatoprotective activity, and it has been proved by different animal models that give many links to develop the future trials.
ACKNOWLEDGEMENT: I am grateful to my Ph.D. guide, Dr. Priya Jain, Faculty of Pharmacy, SAGE University, for giving me support to carry on my work.
CONFLICTS OF INTEREST: There are no conflicts of interest.
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How to cite this article:
Saiju P, Jain P and Chatterjee DP: Present scenario of hepatoprotective potential of medicinal plants: an updated review. Int J Pharm Sci & Res 2020; 11(9): 4189-00. doi: 10.13040/IJPSR.0975-8232.11(9).4189-00.
All © 2013 are reserved by the International Journal of Pharmaceutical Sciences and Research. This Journal licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License.
P. Saiju *, P. Jain and D. P. Chatterjee
Faculty of Pharmacy, SAGE University, Indore, Madhya Pradesh, India.
06 December 2019
26 February 2020
11 March 2020
01 September 2020