水飞蓟宾通过AMPK/Nrf2/NF-κB通路互作调控大口黑鲈高能饲料诱导的肝肠氧化应激与脂代谢紊乱

本研究揭示了水飞蓟宾(Si)作为功能性饲料添加剂，通过激活AMPK/Nrf2通路抑制NF-κB炎症信号，有效缓解高碳水化合物(HC)和高脂肪(HF)饲料导致的生长抑制、肝脂沉积和肠屏障损伤，为水产养殖中代谢综合征防控提供了新型营养干预策略。

　　

Highlight

水飞蓟宾通过饮食依赖的双重调控途径改善大口黑鲈生长并抑制代谢综合征

碳水化合物在饲料生产中常被过量添加，而鱼类对碳水化合物的消化效率低于哺乳动物。本实验室前期研究证实，当大口黑鲈日粮中添加18% α-淀粉时会抑制生长。养殖鱼类因饲料营养摄入失衡导致的脂肪过度积累会引发脂代谢紊乱、氧化应激和免疫力下降，这些紊乱可表现为代谢综合征样症状。

Silybin improves growth and inhibits metabolic syndrome induced by HC and HF diets in largemouth bass via a diet-dependent dual regulatory pathway

Carbohydrates are often added in excess during feed production, and fish are less efficient at digesting carbohydrates than mammals. Previous studies in our laboratory have also shown that growth is inhibited when up to 18% α-starch is added to largemouth bass rations. Excessive fat accumulation in cultured fish due to imbalanced nutrient intake in feed leads to lipid metabolism disorders, oxidative stress, and decreased immunity in fish. These disorders can manifest as a metabolic syndrome-like condition.

Conclusion

研究证实，膳食补充100 mg/kg水飞蓟宾通过AMPK/Nrf2/NF-κB通路互作，有效逆转高能饲料对大口黑鲈幼鱼的不利影响，恢复生长性能至对照组水平，调控脂质代谢并减轻氧化应激和炎症反应。这些发现突显了水飞蓟宾在改善脂质周转和维持肝肠氧化还原/免疫稳态方面的双重调节作用，为其作为水产饲料添加剂的应用提供了实践依据。

The study demonstrates that dietary silybin supplementation (100 mg/kg) effectively counteracts the adverse effects of high-energy diets in juvenile largemouth bass by restoring growth performance to control levels, modulating lipid metabolism, and reducing oxidative stress and inflammation through AMPK/Nrf2/NF-κB crosstalk. These findings highlight silybin's dual regulatory role in improving lipid turnover and maintaining hepato-intestinal redox/immune homeostasis, providing practical evidence for its application as an aquafeed additive.