摘要
目的:观察大黄素对四氯化碳(CCl4)诱导肝纤维化大鼠肝脏组织Smad3 mRNA和蛋白表达的影响。方法:50只雄性SD大鼠随机分为空白对照组(10只)、CCl4组(20只)和大黄素+CCl4组(20只),共3组。CCl4皮下注射诱导大鼠肝纤维化模型,同时大黄素灌胃干预,12周后处死大鼠。采用VG胶原染色法检测大鼠肝脏组织病理学改变,免疫组织化学法检测肝脏组织Smad3蛋白表达,实时定量RT-PCR检测肝脏组织Smad3 mRNA表达。结果:与CCl4组比较,大黄素可显著降低CCl4诱导的肝纤维化程度(P<0.05),减少肝脏组织Smad3蛋白和mRNA表达(P<0.05)。结论:大黄素可有效地逆转实验性大鼠肝纤维化,其机制可能通过下调Smad3 mRNA和蛋白表达有关。
Objective： To investigate the inhibitory effects of emodin on hepatic fibrosis induced by carbon tetrachloride （CCl4）, and examine its effects on the expression of Smad3. Methods： Fifty male SD rats were randomly divided into 3 groups, named as blank control group（n=10）, CCl4 group（n=20）, and emodin ＋ CCl4 group（n=20）. The rat models of experimental hepatic fibrosis were established by injection with CCl4. The treated rats received emodin via oral administration at a dosage of 20mg.kg-t.d-t at the same time. The liver histopathology was examined by van Gieson＇s（VG） stain, and the mRNA and protein expressions of Smad3 were assessed using RT-PCR and immunohistochemistry. Results： The fibrotic area in emodin ＋ CCl4 group was decreased compared with the CCl4 group（P〈0.05）. The mRNA and protein expression of Smad3 in the CCl4 group was significantly up-regulated than that in the blank control group, and that from CCl4 ＋emodin group was significantly down-regulated than in the CCl4 group（P〈0.05）. Conclusion： Emodin exerted anti-hepatic fibrosis effect in rats via down-regulation expression of Smad3 in fibrotie liver tissue.
出处
《中华中医药杂志》
CAS
CSCD
北大核心
2013年第2期529-531,共3页
China Journal of Traditional Chinese Medicine and Pharmacy
基金
黑龙江省教育厅科学技术研究面上项目(No.11551551)~~
