Jia Rui, Hou Yiran, Zhang Liqiang, Li Bing, Zhu Jian
Key Laboratory of Integrated Rice-Fish Farming Ecology, Ministry of Agriculture and Rural Affairs, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi 214081, China.
Wuxi Fisheries College, Nanjing Agricultural University, Wuxi 214081, China.
Antioxidants (Basel). 2024 Apr 29;13(5):548. doi: 10.3390/antiox13050548.
Berberine, a natural alkaloid found abundantly in various medicinal plants, exhibits antioxidative, anti-inflammatory, and lipid metabolism-regulatory properties. Nonetheless, its protective effects and the molecular mechanisms underlying liver injury in fish have not been fully elucidated. The aims of this study were to investigate the antioxidative, anti-inflammatory, and lipid metabolism-regulating effects of berberine against high-fat diet (HFD)-induced liver damage and to clarify the underlying molecular mechanisms. Tilapia were fed diets containing two doses of berberine (50 and 100 mg/kg diet) alongside high fat for 60 days. The results showed that berberine treatments (50 and/or 100 mg/kg) significantly reduced elevated aminotransferases, triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-c) in the plasma. In the liver, berberine treatments significantly increased the expression of peroxisome proliferator-activated receptor α () and carnitine palmitoyltransferase 1 () genes, leading to a reduction in lipid accumulation. Meanwhile, berberine treatment suppressed lipid peroxidation formation and enhanced antioxidant capacity. Berberine upregulated the mRNA levels of erythroid 2-related factor 2 () and its downstream genes including heme oxygenase 1 () and glutathione-S-transferase (). Additionally, berberine attenuated the inflammation by inhibiting the expression of toll-like receptor 2 (), myeloid differential protein-88 (), , and inflammatory cytokines such as interleukin-1β (), tumor necrosis factor-α (), and . In summary, this study suggested that berberine offers protection against HFD-induced liver damage in tilapia via regulating lipid metabolism, antioxidant status, and immune response. This protective effect may be attributed to the modulation of the Nrf2, TLR2/MyD88/NF-κB, and PPARα signaling pathways.
小檗碱是一种在多种药用植物中大量存在的天然生物碱,具有抗氧化、抗炎和脂质代谢调节特性。尽管如此,其对鱼类肝脏损伤的保护作用及潜在分子机制尚未完全阐明。本研究旨在探讨小檗碱对高脂饮食(HFD)诱导的肝脏损伤的抗氧化、抗炎和脂质代谢调节作用,并阐明其潜在分子机制。罗非鱼被喂食含有两种剂量小檗碱(50和100毫克/千克饲料)的高脂饲料60天。结果表明,小檗碱处理(50和/或100毫克/千克)显著降低了血浆中升高的氨基转移酶、甘油三酯(TG)、总胆固醇(TC)和低密度脂蛋白胆固醇(LDL-c)。在肝脏中,小檗碱处理显著增加了过氧化物酶体增殖物激活受体α(PPARα)和肉碱棕榈酰转移酶1(CPT1)基因的表达,导致脂质积累减少。同时,小檗碱处理抑制脂质过氧化形成并增强抗氧化能力。小檗碱上调了红细胞2相关因子2(Nrf2)及其下游基因包括血红素加氧酶1(HO-1)和谷胱甘肽-S-转移酶(GST)的mRNA水平。此外,小檗碱通过抑制Toll样受体2(TLR2)、髓样分化蛋白88(MyD88)、NF-κB以及白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)等炎性细胞因子的表达减轻炎症。总之,本研究表明小檗碱通过调节脂质代谢、抗氧化状态和免疫反应对罗非鱼HFD诱导的肝脏损伤提供保护。这种保护作用可能归因于对Nrf2、TLR2/MyD88/NF-κB和PPARα信号通路的调节。