摘要
目的:探讨白黎芦醇体外抗肝纤维化的作用机制。方法:原位灌流分离大鼠肝细胞,以维生素E作阳性对照,检测不同浓度白黎芦醇对四氯化碳(CCl4)损伤后肝细胞中丙二醛(MDA)、丙氨酸氨基转移酶(ALT)活性和肝细胞存活率的影响;并用肝星状细胞(HSC)与次氮基三醋酸铁共同培养产生氧应激后,检测不同浓度白黎芦醇对HSC增殖和Ⅰ型胶原生成的影响,并测定细胞培养液中MDA、超氧化物歧化酶(SOD)活性。结果:白黎芦醇明显改善CCl4损伤后肝细胞存活率,抑制CCl4引起的ALT、MDA活性升高,并能明显抑制HSC氧应激后MDA活性升高和SOD活性的降低,抑制HSC增殖和Ⅰ型胶原的生成。结论:白黎芦醇抗肝纤维化作用可能与其抗脂质过氧化有关。
OBJECTIVE： To investigate the mechanism of resveratrol on hepatic fibrosis in vitro. METHODS： The hepatocytes of rats were separated by perfusion in situ. after the rat hepatocyte was injuried by CCh, the level of ALT, MDA and cell viability after cultivation for 3 h were determined respectively; HSC-T were incubated with ferric nitrilotriacetate corn plex（FeNTA） . MTT colorimetry was used for assaying proliferation of HSC. Collagen type Ⅰ accummulation in the culture media was measured by ELISA. Intracellular malonildialdehyde（MDA） , SOD level in the culture media were measured by their reagent boxes. RESULTS：Resveratrol significantly improved cell viability, inhibited the increase of ALT, MDA induced by CCl4; HSC incubation with FeNTA resulted in a significant production of intracellular MDA associated with decrease SOD activity .Exposure of HSC to FeNTA significantly enhanced the number of proliferating HSC and collagen type Ⅰ levels in the culture medium. All these effects were reversed by the antioxidant resveratrol. CONCLUSION ：The mechanism of resveratrol on fibrosis mav be related to inhibit lipid peroxidation.
出处
《中国药房》
CAS
CSCD
北大核心
2007年第4期265-266,共2页
China Pharmacy
