Mangiferin exerts hepatoprotective activity against D-galactosamine induced acute toxicity and oxidative/nitrosative stress via Nrf2–NFκB pathways

Das, Joydeep; Ghosh, Jyotirmoy; Roy, Ajitesh; Sil, Parames C.

doi:10.1016/j.taap.2012.01.015

Cited by 154 publications

(103 citation statements)

References 55 publications

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“…The decreased level of GSH in the present investigation may be due to its increased utilization in protecting ''SH'' containing proteins from lipid peroxides. This observation of decrease in GSH level is in agreement with previous reports (Das et al, 2012;Figure 4. Single cell gel electrophoresis (comet assay) of liver cells.…”

Section: Discussionsupporting

confidence: 94%

Effect of lycopene on oxidative stress induced duringd-galactosamine/lipopolysaccharide-sensitized liver injury in rats

Abdulazeez

Devaki

2013

Pharmaceutical Biology

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Context: Lycopene is a phytonutrient under considerable investigation for its antioxidant benefits in treating diseases like cancer, cardiovascular diseases, osteoporosis and diabetes. Objective: This study explores the effect of lycopene against oxidative damage during experimental hepatitis, induced by D-galactosamine/lipopolysaccharide (D-GalN/LPS). Materials and methods: Experimental rats were pretreated with lycopene intraperitoneally for 6 d (10 mg/kg body weight/day) and then induced by D-GalN/LPS. After induction, the levels of lipid peroxides in serum and liver of control and experimental group of animals were measured. The activities of enzymatic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase and glutathione S-transferase and nonenzymatic antioxidants, such as reduced glutathione, vitamin C and vitamin E were also analyzed. The genotoxic effect of D-GalN/LPS was evaluated through the comet assay. Results: The elevated level of lipid peroxides induced by D-GalN/LPS was significantly (p50.05) reverted in lycopene pretreated animals. Lycopene administration restored (p50.05) the decreased activities of enzymatic and nonenzymatic antioxidant markers during D-GalN/LPS induction. The DNA strand breaks (72.3 mM) generated during D-GalN/LPS toxic injury was significantly reduced (35.5 mM) upon pretreatment with lycopene as observed by reduced tail movement in comet assay. Discussion and conclusion: There is no conclusive report about lycopene-assisted protection against free radical mediated toxic injury induced by D-GalN/LPS. Our findings reveal that lycopene effectively combated oxidative damage and protected antioxidant defense status of the cell. Pretreatment of lycopene also offers protection against the DNA damage and confirms the antioxidant nature of the phytonutreint against experimental hepatitis.

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Section: Discussionsupporting

confidence: 94%

Effect of lycopene on oxidative stress induced duringd-galactosamine/lipopolysaccharide-sensitized liver injury in rats

Abdulazeez

Devaki

2013

Pharmaceutical Biology

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“…It was reported that the hepatotoxicity induced by some compounds (eg. carbon tetrachloride) was associated with changes in NF-jB and proinflammatory cytokines expression (Das et al, 2012;Dorn et al, 2012). In this research, VPA caused an increase in the nuclear level of NF-jB concurrent with induction of IL-1b, IL-6 and TNFa expression.…”

Section: Discussionmentioning

confidence: 66%

Role of Nrf2 activation and NF-κB inhibition in valproic acid induced hepatotoxicity and in diammonium glycyrrhizinate induced protection in mice

Jin

Xiong

Hou

et al. 2014

Food and Chemical Toxicology

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“…Downstream targets of Nrf2 include direct antioxidant proteins (e.g., glutathione peroxidase, heme oxygenase-1 [HO-1], and NAD(P)H:quinone oxidoreductase-1 [NQO1]) and thiol metabolism-associated detoxifying enzymes (e.g., glutathione-S-transferase and glutamate-cysteine ligase) (8). It has been shown that Nrf2-dependent antioxidant proteins exert protective effects in animal models of inflammatory ALF (4,15). Additionally B-cell lymphoma 2 (Bcl-2) activated by Nrf2 exerts anti-apoptotic effects (18).…”

Section: Introductionmentioning

confidence: 99%

Cystathionine γ-Lyase Deficiency Protects Mice from Galactosamine/Lipopolysaccharide-Induced Acute Liver Failure

Shirozu

Tokuda

Marutani

et al. 2014

Antioxidants & Redox Signaling

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Aims: Acute liver failure (ALF) is a fatal syndrome attributed to massive hepatocyte death. Hydrogen sulfide (H 2 S) has been reported to exert cytoprotective or cytotoxic effects. Here, we examined the role of cystathionine clyase (CSE, an enzyme produces H 2 S) in ALF induced by D-Galactosamine (GalN) and lipopolysaccharide (LPS). Results: Wild-type (WT) mice exhibited high mortality rate, prominent liver injury, and increased plasma alanine aminotransferase levels after GalN/LPS challenge. Congenital deficiency or chemical inhibition of CSE by DLpropargylglycine attenuated GalN/LPS-induced liver injury. CSE deficiency markedly improved survival rate and attenuated GalN/LPS-induced upregulation of inflammatory cytokines and activation of caspase 3 and poly (ADP-ribose) polymerase (PARP) in the liver. CSE deficiency protected primary hepatocytes from GalN/tumor necrosis factor-a (TNF-a)-induced cell death without affecting LPS-induced TNF-a production from primary peritoneal macrophages. Beneficial effects of CSE deficiency were associated with markedly elevated homocysteine and thiosulfate levels, upregulation of NF-E2 p45-related factor 2 (Nrf2) and antioxidant proteins, activation of Akt-dependent anti-apoptotic signaling, and inhibition of GalN/LPS-induced JNK phosphorylation in the liver. Finally, administration of sodium thiosulfate (STS) attenuated GalN/LPS-induced liver injury via activation of Aktand Nrf2-dependent signaling and inhibition of GalN/LPS-induced JNK phosphorylation in WT mice. Innovation: These results suggest that inhibition of CSE or administration of STS prevents acute inflammatory liver failure by augmenting thiosulfate levels and upregulating antioxidant and anti-apoptotic defense in the liver. Conclusion: Congenital deficiency or chemical inhibition of CSE increases thiosulfate levels in the liver and prevents ALF at least in part by augmentation of antioxidant and anti-apoptotic mechanisms. Antioxid. Redox Signal. 20,[204][205][206][207][208][209][210][211][212][213][214][215][216]

show abstract

Mangiferin exerts hepatoprotective activity against D-galactosamine induced acute toxicity and oxidative/nitrosative stress via Nrf2–NFκB pathways

Cited by 154 publications

References 55 publications

Effect of lycopene on oxidative stress induced duringd-galactosamine/lipopolysaccharide-sensitized liver injury in rats

Effect of lycopene on oxidative stress induced duringd-galactosamine/lipopolysaccharide-sensitized liver injury in rats

Role of Nrf2 activation and NF-κB inhibition in valproic acid induced hepatotoxicity and in diammonium glycyrrhizinate induced protection in mice

Cystathionine γ-Lyase Deficiency Protects Mice from Galactosamine/Lipopolysaccharide-Induced Acute Liver Failure

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