Astragalin Suppresses Colorectal Carcinogenesis by Targeting Proliferation, Oxidative Stress, and Inflammation

Colorectal cancer (CRC) is a leading cause of cancer-related death worldwide. This study evaluated astragalin's (AST) anti-proliferative and chemopreventive effects on CRC.

AST's effects were assessed in vitro on Caco-2 and HT-29 cells and in vivo on azoxymethane (AOM)-induced aberrant crypt foci (ACF) in rats. Rats received AST (50 or 100 mg/kg, 60 days) or 5-fluorouracil (5-FU) (35 mg/kg, 5 days).

AST inhibited Caco-2 and HT-29 cell growth (IC50: 20.15-34.50 µg/mL). In AOM-induced rats, AST reduced ACF formation, improved colon histology, downregulated β-catenin, and upregulated Bax. AST also enhanced superoxide dismutase (SOD) and catalase (CAT) activities, reduced malondialdehyde (MDA) levels, and modulated tumor necrosis factor alpha (TNF-α), interlukin-6 (IL-6), and IL-10 levels.

AST demonstrated chemopreventive activity against CRC by exerting antiproliferative, antioxidant, and anti-inflammatory effects, supporting its potential as a therapeutic agent.