摘要
目的:探讨黄芪多糖对脂多糖诱导体外培养肝损伤的保护作用及其可能的机制。方法:将原代培养的大鼠肝细胞分为正常组、脂多糖模型组和黄芪多糖(25、50、100mg/L)治疗组。药物作用24小时后,MTT法检测细胞存活率;取培养的细胞上清液测门冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)的活性;以ELISA法测定血清中TNF-α、IL-6水平;Western blot测定肝细胞中p65,IκBα表达。结果:脂多糖作用24小时后与正常对照组相比,细胞存活率下降33%,AST、ALT活性增高;TNF-α、IL-6含量增加;p65表达增高而IκBα表达降低。黄芪多糖(25、50、100mg/L)在升高细胞存活率,降低AST、ALT活性的同时,可使脂多糖诱导的TNF-α、IL-6水平含量降低,p65表达降低而IκBα表达增高。结论:黄芪多糖对脂多糖诱导的肝细胞损伤具有保护作用,且这种保护作用可能与黄芪多糖抑制NF-κB通路进而降低炎症因子水平有关。
Objective： The aim of the present study was to study the protective effect of astragalus polysaccharides on LPS-induced hepatocytes injury,and to explore a possible mechanism.Methods： The cultured hepatocytes were divided into 5 groups： the normal group,the model group,and the different does of astragalus polysaccharides groups（25,50,100 mg/L）.After 24 h of incubation,the cell viability rates were detected by MTT;the activity of serum ALT,AST were detected;The content of TNF-α and IL-6 were determined by ELISA;the expression of p65 and IκBα were measured by Western blot.Results： Compared with the normal group,the activity of ALT,AST,the content of TNF-α and IL-6 and the expression of p65 were increased while the expression of IκBα and the viability rates were decreased.APS（25,50,100mg/L） could obviously reduce the activities of ALT,AST,the content of TNF-α and IL-6 and the expression of p65,increased the the expression of IκBα and the viability rates compared with model group.Conclusion： APS has a protective effect on LPS-induced hepatocytes injury,which is partially via attenuating inflammatory effect and the NF-κB signling pathway.
出处
《中药药理与临床》
CAS
CSCD
北大核心
2013年第3期85-88,共4页
Pharmacology and Clinics of Chinese Materia Medica
关键词
黄芪多糖
脂多糖
肝细胞损伤
Astragalus polysaccharides（黄芪多糖） LPS hepatocytes injury
