作者
Zhang, Lanlan,Wang, Panpan,Sun, Ziqi,Su, Defang,Maiwulanjiang, Maitinuer
摘要
This study aimed to investigate the impact of magnoflorine (Mag) on acute exercise-induced fatigue and its underlying mechanisms. Seventy-two male Kunming mice were divided into six groups: a non-treatment control, a vehicle control (ddH2O), a positive control (Gaoshan Hongjingtian Koufuye), and three Mag groups (10, 25, and 50 mg/kg). Antifatigue effects were assessed through organs and body weights, exercise endurance, and biochemical parameters, including superoxide dismutase (SOD), reactive oxygen species (ROS), malonydialdehyde (MDA), catalase (CAT), glutathione peroxidase (GPX), glutathione (GSH), total antioxidant capacity (T-AOC), glycogen, succinate dehydrogenase (SDH), malate dehydrogenase (MDH), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), nitric oxide (NO), and liver tissue histochemistry. Activation of the phosphoinositide-3-kinase/protein kinase B (PI3K/AKT) signaling pathway was evaluated using Western blot. No significant differences were observed in organs and body weights, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, and liver cellular structures. Mag significantly prolonged exercise endurance in Rota-rod and forced swimming tests compared to controls. Mag increased hemoglobin (Hb), testosterone/corticosterone (T/C), and creatine kinase (CK) levels and decreased serum lactic acid (LD), lactate dehydrogenase (LDH), and blood urea nitrogen (BUN). Mag also enhanced glycogen storage, SDH, and MDH levels. Mechanistically, Mag exhibits antioxidant and anti-inflammatory properties in liver tissues and hepatocytes via activation of the PI3K/AKT signaling pathway. Mag alleviated acute exercise-induced fatigue by modulating energy metabolism, antioxidation, and anti-inflammation through the PI3K/AKT signaling pathway. These findings suggest potential therapeutic implications for Mag in combating exercise-induced fatigue and related physiological stressors.