Hepatoprotective effects of resveratrol on α-amanitin-induced liver toxicity in rats

Objective: The hepatoprotective effects of resveratrol against alpha-Amanitin (alpha-AMA)-induced liver toxicity were investigated in an experimental rat model, focusing on oxidative stress, inflammation, apoptosis, and liver function. Methods: Thirty-two male Sprague-Dawley rats were divided into four groups (n = 8 per group): Control, resveratrol, alpha-AMA, and resveratrol+alpha-AMA. The resveratrol group received 20 mg/kg resveratrol orally for 7 days. The alpha-AMA group received 3 mg/kg alpha-AMA intraperitoneally on the 8th day. The resveratrol+alpha-AMA group received 20 mg/kg resveratrol orally (7 days) followed by 3 mg/kg alpha-AMA intraperitoneally on the 8th day. Liver tissues and blood samples were collected 48 h after alpha-amanitin administration for histopathological, immunohistochemical (NFkB, LC3B), and biochemical analyses (GSH, MDA, CAT, GPx, MPO, NOS, AST, ALT). Results: alpha-AMA significantly increased AST and ALT levels, oxidative stress marker (MDA), and inflammatory marker (MPO), while reducing antioxidant levels (GSH, CAT, GPx) and NOS concentration (P < 0.001 for all parameters). Histopathological analysis showed severe liver damage with increased NFkB and LC3B expression. resveratrol treatment significantly reduced AST and ALT levels (P < 0.01 for both parameters), decreased MDA and MPO levels, and increased NOS concentration, GSH, CAT, and GPx levels (P < 0.05 for all parameters). Reduced NFkB and LC3B expression in the resveratrol+alpha-AMA group and showed histopathological improvements. Conclusion: Resveratrol demonstrated substantial hepatoprotective effects against alpha-AMA induced liver toxicity by reducing oxidative stress, inflammation, and apoptosis, and improving liver function. These findings suggest that resveratrol could be a potential therapeutic agent for treating liver damage caused by potent hepatotoxins like alpha-AMA.

Dergi

TOXICON

Yıl

2024

Cilt

247

ISSN

0041-0101

eISSN

1879-3150

DOI

10.1016/j.toxicon.2024.107855

WoS UID

WOS:001274329700001