Dietary silymarin effectively alleviated fumonisin B1-induced hepatopancreatic steatosis and fibrosis in juvenile grass carp (Ctenopharyngodon idella)

脂肪变性 草鱼 生物 伏马菌素 伏马菌素B1 纤维化 毒素 氧化应激 斑马鱼 少年 食品科学 内质网 脂肪酸 内科学 内分泌学 脂质过氧化 氧化磷酸化 细胞凋亡 生物化学 药理学 真菌毒素
作者
Daiyu Chen,Weidan Jiang,Pei Wu,Yang Liu,Yaobin Ma,Hongyun Zhang,Hongmei Ren,Xiaowan Jin,Xiaoqiu Zhou,Lin Feng
出处
期刊:Marine Life Science & Technology [Springer Science+Business Media]
标识
DOI:10.1007/s42995-025-00349-y
摘要

Abstract Fumonisin B1 (FB1) is a widely distributed environmental pollutant that specifically targets the liver, leading to hepatotoxicity. However, there is limited reference data on the hepatotoxicity of FB1 in fish and the corresponding mitigation measures. Silymarin (SIL) is a safe natural plant extract that exhibits hepatoprotective effects. This study aimed to evaluate the influence of supplemented SIL in the diet on FB1-induced hepatopancreatic injury in grass carp ( Ctenopharyngodon idella ). The grass carp (10.92 ± 0.01 g, n = 720) were divided into four groups at random: controls, FB1 (4 mg/kg), SIL (60 mg/kg) and FB1 + SIL group for 30 days. The results indicated that FB1 induced growth inhibition ( P < 0.05), hepatopancreatic damage, steatosis and fibrosis. Dietary SIL alleviated growth inhibition, hepatopancreatic steatosis, accompanied by an increase in the expression levels of molecules related to lipid droplet and mitochondrial interaction ( P < 0.01), as well as the β-oxidation of fatty acids ( P < 0.05). Reduced steatosis mitigated oxidative damage and endoplasmic reticulum stress ( P < 0.05). These changes further relieved the activation of apoptosis ( P < 0.01), which further alleviated the activation of the toll-like receptor 4/NF-kappa B pathway ( P < 0.01) and transforming growth factor/SMAD family member pathway ( P < 0.05), ultimately mitigating hepatopancreatic fibrosis. These results suggested that dietary supplementation with SIL effectively mitigated FB1-induced hepatopancreatic damage. Thus, this study provided new insights into strategies for mitigating FB1-induced hepatotoxicity.
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