摘要
目的:研究莱菔硫烷(SFN)对酒精诱发的肝脏脂肪代谢异常的影响及机制。方法:预先给予雄性C57BL/6小鼠不同剂量的莱菔硫烷,复制急性酒精性肝损伤模型,观察莱菔硫烷对酒精诱发的肝脏脂肪代谢异常的预保护作用,并对可能机制进行分析。结果:莱菔硫烷能显著减轻酒精对肝脏的病理学损伤,并且有明显的剂量依赖性;莱菔硫烷能明显降低酒精引起的血清中甘油三酯(TG)、总胆固醇(CHOL)水平升高,对高密度脂蛋白(HDL)的作用不明显;莱菔硫烷可激活转录因子核因子红系2相关因子2(Nrf2)的表达,使其下游效应因子即Ⅱ相解毒酶谷胱甘肽S-转移酶(GST)活性及抗氧化物谷胱甘肽(GSH)含量均升高;莱菔硫烷能明显降低酒精刺激的固醇调节元件结合蛋白-1c(SREBP-1c)的表达。结论:莱菔硫烷能保护酒精诱导的肝脏脂肪代谢紊乱,其主要作用机制为SFN通过激活Nrf2增强了抗氧化作用,同时通过抑制SREBP-1c,改善了酒精所致的肝脏脂肪代谢的异常。
Objective: To investigate the effects of sulforaphane(SFN) on abnormal lipid metabolism induced by alcohol and its action mechanisms. Methods: Acute liver injury model was established with different doses of SFN in male C57 BL/6 mice. The prevention effect of SFN on abnormal lipid metabolism was observed and its possible mechanism was analyzed. Results: SFN significantly alleviated the damage of the liver caused by alcohol,which showed dose-dependent relationship; it decreased the levels of TG and CHOL,but not HDL; it obviously activated the expression of Nrf2,subsequently induced the activity of phase II enzyme GST and increased the content of GSH; it also down-regulated the expression of SREBP-1 c. Conclusion: SFN can regulate the disorders of lipid metabolism in liver induced by alcohol. The main mechanisms may include the followings: the activation of Nrf2,which enhances the antioxidant capability; and the inhibition of SREBP1 c,which improves the abnormal lipid metabolism.
出处
《中医药学报》
CAS
2018年第1期40-43,共4页
Acta Chinese Medicine and Pharmacology
基金
国家自然科学基金面上项目(81573135)
黑龙江省教育厅科学技术研究项目(12541763)
关键词
莱菔硫烷
急性酒精性肝损伤
脂肪代谢
抗氧化
Sulforaphane
Acute alcoholic-induced liver injury
Lipid metabolism
Antioxidant
