Pyrogallol-induced hepatotoxicity in rats: A model to evaluate
antioxidant hepatoprotective agents

Yk, Gupta; Sharma, Madhuri; Chaudhary, Geeta

doi:10.1358/mf.2002.24.8.705070

Cited by 36 publications

(24 citation statements)

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“…This was evident from the significant normalization of serum AST, ALT, ALP, LDH and bilirubin levels in caffeic acid administered OXT treated rats. The above findings could be correlated with previous studies, which reported that treatment with ferulic acid [24], tetrahydrocurcumin and quercetin [25] significantly reduced the levels of serum markers in drug induced hepatotoxicity [26].…”

Section: Resultssupporting

confidence: 90%

Antioxidant Effect of Caffeic Acid on Oxytetracycline Induced Lipid Peroxidation in Albino Rats

Rajendran

Subash

2010

Ind J Clin Biochem

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Caffeic acid is a well-known phenolic compound widely present in plant kingdom. The aim of this study was to investigate the possible protective effect of caffeic acid (CA) against oxytetracycline (OXT) induced hepatotoxicity in male Albino Wistar rats. A total of 30 rats weighing 150-170 g were randomly divided into five groups of six rats in each group. Oral administration of OXT (200 mg/kg body weight/day) for 15 days produced hepatic damage as manifested by a significant increase in serum hepatic markers namely aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), bilirubin and increased plasma and hepatic lipid peroxidation indices (TBARS and hydroperoxide). The present finding shows that the levels of enzymatic antioxidants namely superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were significantly decreased in OXT intoxicated rats. Upon oral administration of caffeic acid (40 mg/kg body weight/day) there were decreased hepatic marker activities, bilirubin and lipid peroxidation and increased enzymatic antioxidants in OXT ? Caffeic acid group compared to Normal ? OXT group(P \ 0.05). Our study suggests that caffeic acid has antioxidant property and hepatoprotective ability against OXT induced toxicity.

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Section: Resultssupporting

confidence: 90%

Antioxidant Effect of Caffeic Acid on Oxytetracycline Induced Lipid Peroxidation in Albino Rats

Rajendran

Subash

2010

Ind J Clin Biochem

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“…SOD removes superoxide by converting it to H 2 O 2 , which can be rapidly converted to water by CAT and glutathione peroxide, thus participating with other antioxidant enzymes, in the enzymatic defense against oxygen toxicity. In this study, SOD plays an important role in the elimination of ROS(Reactive oxygen species) derived from the peroxidative process of xenobiotics in liver tissues 30 . The observed increase of SOD activity suggests that the Vedic guard treatment has an efficient protective mechanism (P<0.001) in response to ROS.…”

Section: Discussionmentioning

confidence: 99%

Untitled

2010

IJPSR

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The present study was undertaken to evaluate antioxidant and hypolipidemic activity of Vedic guard, a polyherbal formulation comprising of Terminalia arjuna, Withania sominefera, Bacopa monnierii, Tinosporia cardifolia, Commiphora mukul and many other plant extracts, all of which are classifieds in Ayurveda as Rasaayanas which are reported to promote antioxidant and hypolipidemic activity. Antioxidant activity has been established in young adult rats against antitubercular drug induced hepatotoxicity but not in geriatric rats. Antioxidant activity was evaluated by hepatoprotectivity against carbon tetrachloride induced liver toxicity for 21 days in geriatric rats using Silymarin as reference standard, and by pyrogallol induced immunosupression for 28 days in young adult rats using levamisole as reference standard. Hypolipidemic activity was evaluated using triton WR1339 induced hyperlipidemic rats as experimental model in acute study. Oxidative damage was evidenced by occurrence of liver cirrhosis, elevation of AST, ALT, and ALP, total bilirubin in blood serum and increased LPO, reduced CAT and GSH in liver homogenate. Vedic guard treatment in geriatric rats with doses of 90mg/kg, 180mg/kg b. w., p. o. and standard silymarin significantly reversed all the changes that were due to CCl 4. Similarly pyrogallol induced immunosupression was evidenced by increased LPO and decreased GSH, SOD, CAT in liver homogenate. Vedic guard treatment in young adult rats at 180mg/kg b. w., p .o. and standard levamisole significantly altered the changes that were due to immunosupression. Hyperlipidemia was evidenced by increased serum total cholesterol, triglycerides, LDL, VLDL and decreased HDL. Vedic guard treatment with lower and higher doses and standard atorvastatin reversed all changes that were due to hyperlipidemia. The Vedic guard showed significant hypolipidemic and antioxidant activity.

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“…Briefly, 5x10 3 HPF cells per well in 96-well microtiter plates (Nalge Nunc International; Thermo Fisher Scientific, Inc., Penfield, NY, USA) were exposed to 0, 50 or 100 µM PG with or without each MAPK inhibitor at 37˚C for 24 h. Changes in cell viability induced by PG and/or a given MAPK inhibitor were determined by measuring the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT; Sigma-Aldrich; Merck KGaA) dye absorbance as previously described (28).…”

Section: Methodsmentioning

confidence: 99%

“…Despite the useful effects of PG, its toxicity remains a concern for the individuals exposed to it. Multiple studies have been performed to elucidate the toxicological and pharmacological effects of PG (2)(3)(4). However, the molecular mechanisms underlying the cellular effects of PG remain only partially clarified.…”

Section: Introductionmentioning

confidence: 99%

MAPK inhibitors enhance cell death in pyrogallol-treated human pulmonary fibroblast cells via increasing O2•− levels

Han

Park

2017

Oncology Letters

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Abstract. Pyrogallol (PG) induces apoptosis in lung cancer cells via the overproduction of O 2•-and affects mitogen-activated protein kinases (MAPKs) in these cells. The aim of the present study was to elucidate the effect of PG and/or MAPK inhibitors on human pulmonary fibroblast (HPF) cell viability in relation to reactive oxygen species (ROS) and glutathione (GSH). Treatment with 50 or 100 µM PG inhibited the viability of HPF cells, and induced cell death and the loss of mitochondrial membrane potential (MMP; ΔΨ m ). In particular, treatment with 100 µM PG induced cell death via apoptosis as well as necrosis in HPF cells. PG increased mitochondrial O 2•-levels and the number of GSH-depleted HPF cells. All the MAPK (mitogen-activated protein kinase kinase, c-Jun N-terminal kinase and p38) inhibitors enhanced the inhibition of cell viability, cell death and MMP (ΔΨ m ) loss in 100 µM PG-treated HPF cells. All the inhibitors increased the O 2•-levels in 100 µM PG-treated HPF cells, but none of the inhibitors significantly altered the PG-induced GSH depletion. In conclusion, PG treatment induced cell death via apoptosis and necrosis in HPF cells. Treatment with MAPK inhibitors slightly enhanced cell death in PG-treated HPF cells. HPF cell death induced by PG and/or MAPK inhibitors was at least partially associated with changes in O 2•-levels and GSH content. The present data provided useful information to understand PG-induced normal lung cell death in association with MAPK signaling pathways and ROS levels.

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Pyrogallol-induced hepatotoxicity in rats: A model to evaluate antioxidant hepatoprotective agents

Cited by 36 publications

References 0 publications

Antioxidant Effect of Caffeic Acid on Oxytetracycline Induced Lipid Peroxidation in Albino Rats

Antioxidant Effect of Caffeic Acid on Oxytetracycline Induced Lipid Peroxidation in Albino Rats

Untitled

MAPK inhibitors enhance cell death in pyrogallol-treated human pulmonary fibroblast cells via increasing O2•− levels

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