The current study aimed to explore the protective roles of ginseng against dexamethasone liver devastating effects. Sixty male rats were equally allocated into six groups; G1: control, G2: ginseng aqueous extract (200 mg/kg B.W. orally /4 weeks), G3: dexamethasone (1mg/kg B.W. i.p/one week then decapitated), G4: dexamethasone- withdrawal group (1mg/kg B.W. i.p/one week and decapitated at the end of experiment), G5: dexamethasone ginseng treated group (injected with dexamethasone/one week then treated with ginseng/other 3weeks), and G6: ginseng-dexamethasone-ginseng group (received ginseng/two weeks followed by dexamethasone/one week then ginseng/another week). Dexamethasone significantly increased serum liver enzymatic activities alongside with mild to moderate hepatic vacuolation, and periportal mononuclear infiltration suggesting liver damage. The level of hepatic malondialdehyde (MDA) was elevated markedly with subsequent decline in the reduced glutathione concentration following challenged with dexamethasone. Moreover, the hepatic expression of thioredoxin mRNA transcript was down-regulated while BCL2-associated X protein (Bax) mRNA transcript was up-regulated providing imbalance in antioxidant and apoptosis pathway. Ginseng treatment ameliorated the damaged effects of dexamethasone on the liver as indicated by attenuation of elevated liver enzymatic activities, augmentation the reduced glutathione level, up-regulation thioredoxin mRNA transcription along with down-regulation of Bax mRNA expression in liver tissue. Conclusively, ginseng exerted a protective action on dexamethasone hepatic side effects through anti-apoptotic and antioxidant properties.
Key words: Antioxidant; Apoptosis; Dexamethasone; Glutathione; Hepatic damage; Thioredoxin
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