Nicorandil attenuates thioacetamide induced liver fibrosis via AMPK, SIRT1 and HIF1α mediated cellular energy homeostasis.

ABSTRACT: Liver fibrosis, marked by excessive extracellular matrix deposition and chronic inflammation, is a significant health concern that can progress to cirrhosis and liver failure. Current treatments are limited, highlighting the need for novel therapies. Nicorandil (NIC), a potassium channel opener with nitric oxide-donating properties, has shown cytoprotective and anti-inflammatory effects. This study evaluates the efficacy of NIC in attenuating thioacetamide (TAA)-induced liver fibrosis in rats, focusing on the AMPK/SIRT-1/HIF-1α signaling pathway. Twenty-four adult male albino rats were randomly assigned to four groups: a control group, a TAA-treated group, and two groups treated with NIC at doses of 7.5 mg/kg/day and 15 mg/kg/day, respectively, for six weeks. TAA was administered intraperi

SUBMITTER: Kozman MR 

PROVIDER: S-EPMC12695948 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature