乙酰半胱氨酸对四氯化碳诱导的原代培养大鼠肝细胞损伤的保护作用

Hepatoprotective Effects of N-acetylcysteine Injection on Tetrachloride-induced Injury in Primary Rat Hepatic Cells

关键词:  乙酰半胱氨酸  保肝  原代培养  大鼠肝细胞  四氯化碳损伤

Key words:  N-acetylcysteine  hepatoprotective effect  primary culture  rat hepatic cell  tetrachloride-induced injury

摘要:

目的 观察乙酰半胱氨酸(NAC)对四氯化碳(CCl4)诱导的原代培养大鼠肝细胞损伤的作用。方法 在24孔细胞培养板上，用CCl4诱导原代培养肝细胞损伤，分别加入不同浓度的NAC，培养20 h后，测定上清液谷草转移酶(AST)活性，并MTT法检测细胞活力。结果 NAC在100 μmol·L^-1内，对正常培养的大鼠肝细胞没有影响；在4~100 μmol·L^-1内，NAC能剂量依赖性地抑制CCl4诱导的肝细胞活性的降低，EC50约为20 μmol·L^-1；当浓度为100 μmol·L^-1时，可以逆转CCl4诱导的肝损伤，使肝细胞释放AST降到接近正常水平，并明显改善肝细胞形态学变化。结论 NAC对CCl4诱导的肝损伤具有保护作用。

Abstract:

OBJECTIVE To investigate the effects of N-acetylcysteine (NAC) injection on tetrachloride (CCl4)-induced injury in primary rat hepatic cells. METHODS Primary cultured hepatic cells were induced injury by CCl4. The cells were incubated with NAC(100, 20, 4 μmol·L^-1) for 20 h. The expressions of aspartate transaminase(AST) in hepatic cells were determined by MTT assay. RESULTS After incubated with NAC for 20 hours, neither viability of primary rat hepatic cells decreases significantly, nor released AST from hepatic cells increases significantly in medium. However, in 4-100 μmol·L^-1, NAC reversed concentration-dependently the CCl4-decreased viability, and the EC50 was about 20 μmol·L^-1; in 100 μmol·L^-1, NAC inhibited effectively CCl4-increased AST in primary rat hepatic cells, and attenuated obviously the change of hepatic cell morphous. CONCLUSION NAC has a protective effect on tetrachloride-induced injury.