RETRACTION: Bees' Honey Attenuation of Metanil-Yellow-Induced Hepatotoxicity in Rats

Objective The current study evaluated the hepatoprotective activity of Curcuma vamana ethanolic rhizome extract against paracetamol and CCl4 induced hepatotoxicity in a rat model.Materials and methods Hepatoprotective activity of Curcuma vamana was evaluated on CCl4 and paracetamol induced hepatotoxicity in rats by measuring levels of biochemical enzymes in the serum and tissue homogenate and histopathological assessment.Results The in-vivo hepatoprotective activity of different doses 100 200 400mgkg of ethanol rhizome extract of Curcuma vamana was carried out against CCl4 and paracetamol induced hepatotoxicity in rats. During the study it was found the EECV showed significant plt0.001 decrease in the biochemical enzymes in serum and tissue homogenate such as AST ALT ALP TB LDL-cholesterol Total cholesterols LPO and significantly increases the HDL- cholesterol Total protein Glucose GSH CAT SOD and total thiols levels as compared to the control groups were supported these findings further histopathological studies. Thus the present finding provides scientific evidence of to the ethno-medicinal value of rhizome of Curcuma vamana in liver disorders.Conclusion In conclusion Curcuma vamana possesses a significant hepatoprotective activity against CCl4 and paracetamol induced hepatotoxicity in rats.

Study of Silymarin on Ethanol Induced Hepatotoxicity and Expression of Bcl-2, Bax and p53 Levels

Hepatoprotective Action of Dehydrozingerone in Carbon Tetrachloride and Thioacetamide-induced Hepatotoxicity in Wistar Rats

Recently, melatonin has attracted attention because of their strong free radical scavenging and antioxidant properties. The present study was designed to investigate the role of melatonin against cypermethrin induced hepatotoxicity in rats using qualitative, quantitative and biochemical approaches. Adult female Wistar rats were randomly divided into four groups; each group consists of six animals. Control group received vehicle, corn oil; Cypermethrin (CM) (250mg/kg bw); Melatonin (MEL) (10 mg/kg bw); CM+MEL treated group. Animals were treated orally, daily for a period of 4 weeks. Animals were sacrificed by decapitation and liver was used for various biochemical and histopathological examinations. The result of this study shows that in vivo administration of cypermethrin caused a significant induction of oxidative damage in liver tissue as evidenced by depletion of proteins, glutathione (GSH) and increased lipid peroxidation in hepatic tissue. Cypermethrin administration significantly enhanced the activities of enzymatic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) glutathione reductase (GR) and glutathione-S- transferase (GST). Cypermethrin intoxication exhibited elevation in the activities of liver marker enzymes such as serum glutamate pyruvate transaminase (SGPT) serum glutamate oxaloacetate transaminase (SGOT) and Lactate dehydrogenase (LDH). Furthermore, the co-administration of melatonin mitigates the hepatotoxicity of cypermethrin by normalizing the biochemical and enzymatic parameters. The biochemical observations were supported by histopathological examination of liver. The findings of this investigation suggest that the melatonin may play a protective role against cypermethrin induced hepatotoxicity and oxidative damage in female albino rats.

Globally mercury (Hg) has been reported as one of heavy metal of known toxicity, noted for inducing public health disasters. Present study examines the therapeutics potentials of Ocimum basilicum on mercury chloride (HgCl2) induced hepatotoxicity in Wistar rats. Thirty adult Wistar rats randomly divided into six groups (A-F) of five rats each. Group A served as control was given 2 mL/day of distilled water, Group B, C, D, E and F received 500 mg/kg body weight (bwt) of O. basilicum extract, 20 mg/kg/bwt of HgCl2, 40 mg/kg bwt of HgCl2, 20 mg/kg bwt of HgCl2 and 500 mg/kg bwt O. basilicum leave extract, 40 mg/kg bwt and 500 mg/kg bwt O. basilicum administered daily by gastric gavage, for 21 consecutive days. The gross anatomical parameters of the liver and liver histology were assessed. Liver oxidative stress was evaluated by liver superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH) and malondialdehyde (MDA) assays. The activities of the biomarker enzymes of the liver (alanine transaminase, aspartate transaminase and alkaline phosphatase were assayed). Histological profiles of the liver revealed derangement of the liver cytoarchitecture following consumption of mercury chloride and a marked improvement was observed after O. basilicum administration. Similarly, O. basilicum improved the reduction of antioxidant parameters (SOD, CAT, GPx and GSH) and the increased MDA caused by mercury chloride consumption. O. basilicum thus proffer protection against free radical mediated oxidative stress in mercury chloride-induced hepatotoxicity in rats.

Ginger (Zingiber officinale) is used traditionally for many therapeutic purposes. .Oxidative stress may be the main reason behind most histological and cellular effects of lead.The aim of this study was to investigate the possible hepatoprotective role of ginger against lead acetate induced hepatotoxicity in rats. .In the present investigation, lead acetate (200 mg/kg b.wt) was given orally to male rats for eight weeks to induce hepatotoxicity.The ginger was found to contain zingerone, gingerdiol, zingibrene, gingerols and shogaols.Lead-induced oxidative stress in liver tissue was indicated by significant decreased levels of liver reduced glutathione (GSH) and superoxide dismutase (SOD).Histologically, the liver showed several histological alterations such as degeneration of hepatocytes by necrosis and apoptosis, fatty changes and inflammatory cells infiltration.Ginger-I (200 mg/kg b.wt) and Ginger-II (300 mg/kg b.wt) markedly attenuated the previous leadinduced biochemical alterations in liver tissues as well as the histological and cellular changes.From this study, it can be concluded that the Zingiber officinale showed effective hepatoprotective and antioxidative action against lead acetate-induced hepatotoxicity in rats.

The potential involvement of sulfite, an obligatory intermediate in the metabolism of carbon disulfide (CS2) to sulfate, in CS2-induced hepatotoxicity in phenobarbital-pretreated rats was investigated. The activity of mitochondrial sulfite oxidase, which is the primary route for the oxidation of sulfite to sulfate, was decreased 78% by a regimen consisting of a low molybdenum diet and drinking water supplemented with tungstate. These rats also had 30% less cytochrome P-450 than those maintained on the control regimen. The dietary regimen did not enhance CS2-induced toxicity but, rather, provided some degree of protection, which was probably due to the decreased amount of cytochrome P-450. Hence, sulfite does not appear to be involved in CS2-induced hepatotoxicity in the rat.

Traditional remedies employ herbal drugs for the treatment of liver ailments and hepatoprotection. Thus, the present study was designed to evaluate the hepatoprotective effect of "extract of Anacyclus pyrethrum Linn" (APE) against antitubercular drug-induced hepatotoxicity in rats. Group I rats (normal control) received vehicle (1 % CMC), while group II rats (hepatotoxic control) isoniazid (INH) plus rifampicin (RIF) each 50 mg/kg/day po, for 28 days. Group III, IV and V rats were administered with APE 200, APE 400 and silymarin 100 mg/kg/day po, respectively, for 28 days. Concurrently, hepatotoxicity was tried to induce by coadministration of INH and RIF each 50 mg/kg/day po for 28 days in group III, IV and V rats. After 24 h of the last dosing, blood was obtained under light anesthesia and the rats were killed. Hepatoprotective effect was assessed by liver weight, relative liver weight and biochemical parameters such as serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), serum bilirubin, cholesterol, total protein and albumin levels. Group IV rats showed significant (p<0.01) decrease in SGPT, SGOT, ALP, LDH, cholesterol, serum bilirubin, liver weight and relative liver weight Levels, while significant (p<0.01) increase in final body weight (b. wt.), total protein and albumin levels as compared to group II rats. Hepatoprotective effect of APE 400 mg/kg/day was comparable to that of silymarin 100 mg/kg/day and the hepatic marker levels were also restored. Hepatoprotective effect of APE was well supported by the histopathological results. Hydroalcoholic APE root possesses hepatoprotective activity as it exhibited the protective effect against INH plus RIF-induced hepatotoxicity in rats.

Hepatoprotective effects of Alpinia officinarum rhizome extract on cisplatin-induced hepatotoxicity in rats: A biochemical, histopathological and immunohistochemical study

Ganoderic acid -loaded solid lipid nanoparticles ameliorate d-galactosamine induced hepatotoxicity in Wistar rats

Background: liver is highly susceptible to the toxic and adverse effects of various metabolites and xenobiotics such as alcohol etc. Alcohol abuse leads to hepatotoxicity that is presented in the form of Alcoholic Liver Disease. Aims and Objectives: The present study was conducted to evaluate hepatoprotective activity of polyherbal formulation. The test drug was studied in comparison with marketed formulations in ethanol induced hepatotoxicity in wistar albino rats. Methods: Total 7 groups of animals were studied comparatively to evaluate efficacy of various formulations. Results: It was found that all the formulations tested including all the dosages of Polyherbal Capsule significantly reduced levels of SGOT (Serum glutamic oxaloacetic transaminase), SGPT (Serum glutamate pyruvate transaminase), Alkaline phosphatase (ALP) and Total Bilirubin when compared to ethanol group. There was significant increase in total protein level in Ariliv Tablet, Silymarin and marketed formulation groups. Also, all the formulations tested effectively preserved the structural integrity of the hepatocellular membrane and liver cell architecture damaged by ethanol. When compared between formulation groups there was no statistical significant difference. Conclusion: It can be concluded that Polyherbal Capsule possesses hepatoprotective activity in ethanol induced hepatotoxicity in rats. Polyherbal Capsule can be effectively used in hepatitis caused due to alcohol.

An experimental study was conducted to evaluate the hepatoprotective effect of aqueous extract of Camellia sinensis or green tea extract and N-acetyl-L-cysteine in acetaminophen-induced hepatotoxicity in rats. Male Wistar rats (n=24) of 3 mon age were equally divided into 4 groups. Group 1 served as normal control. Hepatotoxicity was induced in the remaining three groups with oral administration of 500 mg/kg of acetaminophen from day 1 to day 3. Groups 2, 3 and 4 were subsequently administered orally with distilled water, 300 mg/kg of N-acetyl-L-cysteine and 100 mg/kg green tea extract, respectively for 11 days. Mean body weights and biomarkers of hepatotoxicity were estimated on days 0, 4 (confirmation of toxicity) 15 (at the end of treatment). Hematological parameters were evaluated on 4 and 15 d. Antioxidant profile and ATPase enzymes were assessed at the end of the experiment. Livers were subjected to histopathology and transmission electron microscopy after the sacrifice on day 15. Antioxidant profile, ATPase, hematological and serobiochemical parameters were significantly altered and histopathological changes were noticed in liver of toxic control group. These changes were reversed in groups 3 and 4 that were administered with N-acetyl-L-cysteine and green tea extract, respectively. The results of the present investigation enunciated that green tea extract has potent hepatoprotective activity, though N-acetyl-L-cysteine was found superior in restoring the pathological alterations in acetaminophen-induced hepatotoxicity in Wistar rats.

Objective: The main objective of our study is to see the hepatoprotective effect of Nigella sativa in Cyclosporine induced hepatotoxicity in rats. Methods: the effect of Nigella sativa on cyclosporine induced hepatotoxicity was studied in albino rats. The animals were divided into 3 groups with 6 rats in each group. Group I served as vehicle control, Group II animals were given Cyclosporine 25mg/Kg body weight orally for 21 days and Group III were given Cyclosporine 25mg/Kg + Nigella sativa 1ml/Kg body weight orally for 21 days. The blood samples were collected for liver enzymes estimation before and after the experiment. The animals were sacrificed on 22 nd day and liver was subjected to histopathological examination. Results: Cyclosporine provoked hepatotoxicity was evident from increase of hepatic enzyme levels and histopathological changes. Addition of Nigella sativa has resulted in the decrease of elevated hepatic enzyme levels and improvement in histopathological changes in liver. Conclusion: The present study showed that Nigella sativa oil has protective effect on Cyclosporine induced hepatotoxicity in albino rats.

Cadmium (Cd) is a ubiquitous non-essential environmental and industrial toxicant that affects various organs in humans and experimental animals. Robust evidence confirms the contribution of oxidative stress to the pathogenesis of Cd-induced hepatic damage. Potent polyphenols found in virgin coconut oil (VCO) are free radical scavengers that may be beneficial against Cd hepatotoxicity. Thus, we aimed to evaluate the possible protective effect of polyphenols isolated from VCO on Cd-induced hepatotoxicity and oxidative stress in rats. Rats were pretreated with polyphenols isolated from VCO (10, 20, and 50 mg/kg, orally) 2 weeks prior to concurrent Cd administration (5 mg/kg, orally) for 5 weeks. Subsequently, liver damage, hepatic oxidative stress, and histopathological alterations were evaluated. In vitro antioxidant assays (DPPH and FRAP) were carried out on VCO polyphenols. Cadmium induced liver damage demonstrated by significant alterations in serum markers of liver damage, as well as pronounced decrease in albumin and total protein compared to control. Further, Cd remarkably depressed hepatic activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione (GSH) content. Hepatic lipid peroxidation was markedly increased as highlighted by malondialdehyde (MDA) content. Sub-chronic administration of VCO polyphenols to Cd-treated rats produced a significant hepatoprotective effect and restored hepatic oxidative stress markers comparable to control. The prominent improvement in histopathology of rat liver confirmed the biochemical findings. The findings suggest potential beneficial effect of VCO polyphenols on Cd-induced hepatotoxicity and oxidative stress in rats; the mechanism underlying this action is associated with improvement in antioxidant defense system.

A multi-herbal combination (MHC) of five herbs, namely Punica granatum L., Putranjiva roxburghii Wall., Swertia chirata Buch.-Ham., Tinospora cordifolia (Willd.) Miers and Trigonella corniculata L. was assessed against the paracetamol-induced acute hepatotoxicity in female Wistar rats. The animals were randomly assorted into seven groups with six animals in each group. The rats were pre-treated with MHC (50, 100, and 200 mg/kg bw) and silymarin (50 mg/kg bw) once daily for seven consecutive days via oral route followed by administration of paracetamol (3 g/kg bw) on day 7, an hour after the last administration of MHC and silymarin. It was observed that MHC administration significantly (p ≤ 0.05) overturned the paracetamol-induced increase in serum liver function biomarkers (serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, alkaline phosphatase, and total bilirubin), phase I reaction enzymes (NADPH-cytochrome P450 reductase and NADH-cytochrome b5 reductase), and oxidant biomarkers (lactate dehydrogenase, lipid peroxidation, lipid hydroperoxides, and protein content). MHC administration also reinstated the paracetamol-induced significant decrease (p ≤ 0.05) in haematological indices (haematocrit, haemoglobin, red and white blood cells, and platelets), phase II reaction enzymes (glutathione-S-transferase and DT-diaphorase), membrane-bound enzymes (Na+/K+-ATPase, Ca2+-ATPase, and Mg2+-ATPase), and antioxidant biomarkers (reduced glutathione, superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase). Overall, MHC at 200 mg/kg bw dose significantly (p ≤ 0.05) sheltered the red blood cells from the assault of free radicals, stabilized the structural and functional integrity of hepatocytes, hindered acetaminophen (APAP) biotransformation to its toxic metabolites, and endorsed conjugating abilities to detoxify toxic entities. Furthermore, MHC significantly (p ≤ 0.05) activated enzymatic machinery to scavenge/inhibit the formation of reactive oxygen species, regulated nucleic acid metabolism, surface potential, and membrane fluidity, attenuated tissue breakdown, quenched peroxyl radicals, and provided protection against tissue injury. The necroinflammatory scores revealed strong evidence of MHC (200 mg/kg bw) effectiveness against the paracetamol-induced hepatotoxicity in rats at p ≤ 0.05. The synergistic effect of major inherent phytoconstituents (kaempferol, ellagic acid, and gallic acid), detected by HPLC-PDA, in MHC might have overturned the paracetamol-induced biochemical toxic alterations in rat liver.