摘要
目的研究麝香保心丸对大鼠免疫性肝纤维化的抑制作用及其机制。方法雄性SD大鼠制备免疫性肝纤维化模型,随机均分为模型组,麝香保心丸低、高剂量(22.5、45 mg/kg)组,另设对照组。麝香保心丸组大鼠每天ig给药1次,连续给药10周。第10周末处死大鼠,HE染色法观察各组大鼠肝组织病理改变;RT-PCR法检测肝组织血管内皮生长因子(VEGF)基因表达;免疫组化法检测VEGF、α-肌动蛋白(α-SMA)蛋白的表达;并测定肝组织中丙二醛(MDA)的量和超氧化物歧化酶(SOD)的活性以及胶原纤维面积的变化。结果与模型组相比,麝香保心丸低、高剂量可减轻大鼠肝纤维化程度,显著降低肝组织VEGF基因、VEGF、α-SMA蛋白的表达(P<0.01),显著降低肝组织MDA的量和胶原纤维面积百分比(P<0.05、0.01),使SOD活性增强(P<0.05、0.01),并呈剂量相关性。结论麝香保心丸可减少免疫性肝纤维化大鼠肝纤维化组织中VEGF表达,降低氧化应激反应,进而发挥抗肝纤维化作用,其作用可能通过抑制肝星状细胞活化而实现的。
Objective To study the inhibitory effect of Shexiang Baoxin Pill （SBP） on the immunological liver fibrosis and its possible mechanisms. Methods Male rats with immunological liver fibrosis were equally divided into control, model, and low- and high-dose （22.5 and 45 mg/kg） SBP groups. Rats in SBP groups were ig given SBP once daily for consecutive 10 weeks. On the week 10, all rats were sacrificed and a part of liver tissues were preserved. The changes of hepatic histopathology were observed using HE staining. Gene expression of vascular endothelial growth factor （VEGF） was observed using RT-PCR. The protein expression of VEGF and α-SMA was detected using immunohistochemistry, and MDA content, SOD activity, and the area of collagen fiber in the liver before and after treatments were measured. Results Compared to the model control, low- and high-dose SBP groups could relieve the degree of hepatic fibrosis （P 〈 0.01, 0.05）, reduce the expression of hepatic VEGF mRNA, VEGF, α-SMA （P 〈 0.01）, obviously reduce MDA content and the area of collagen fiber （P 〈 0.05, 0.01）, and increase the activity of SOD （P 〈 0.05, 0.01）. All the effects were dose-dependent. Conclusion SBP may decrease the expression of hepatic VEGF and reduce the level of oxidative stress. The inhibitory effect may depend on its dose, which may be based on inhibiting the activation of hepatic stellate cells.
出处
《中草药》
CAS
CSCD
北大核心
2013年第18期2563-2568,共6页
Chinese Traditional and Herbal Drugs
关键词
麝香保心丸
免疫系统肝纤维化
血管内皮生长因子
氧化应激
肝星状细胞
Shexiang Baoxin Pill
immunological liver fibrosis
vascular endothelial growth factor
oxidative stress
hepatic stellate cells
