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作 者:刘莎[1] 杨林 蒲晓东[1] 巫静娴[3] 张义兵[1] 曹维国[1]
机构地区:[1]重庆医科大学中医药学院,重庆401331 [2]重庆市药品检验所,重庆400015 [3]重庆医科大学基础医学院,重庆400016
出 处:《中国实验方剂学杂志》2011年第13期174-177,共4页Chinese Journal of Experimental Traditional Medical Formulae
基 金:重庆市教委科学技术研究项目(KJ090311)
摘 要:目的:观察三甲散对实验性肝纤维化大鼠转化生长因子(TGF-β)、肝再生增强因子(ALR)的影响,从分子生物学角度探讨其作用机制。方法:SD大鼠100只,50%CCl4植物油溶液ip造模后分为模型组、马洛替酯组(0.1 g·kg-1)及三甲散低、中、高(0.45,0.9,1.8 g·kg-1)剂量组,并设空白组作为对照。给药8周,测定各组大鼠的转氨酶、羟脯氨酸(Hyp)及血清透明质酸(HA)、层黏蛋白(LN)、三型前胶原(PⅢNP)、四型胶原(PⅣP),肝组织TGF-β,ALR的含量;肝组织做病理形态学检查。结果:模型组大鼠转氨酶升高,血清HA,LN,PⅢNP,PⅣP升高,肝组织TGF-β,ALR急剧升高,与空白对照组比较,差异非常显著(P<0.01),病理显示模型组大鼠汇管区及小叶间大量纤维增生。三甲散各剂量组均可降低转氨酶及血清HA,LN,PⅢNP,PⅣP,肝组织TGF-β,ALR含量下降,与模型组比较,差异显著(P<0.05)。结论:三甲散可降低肝纤维化大鼠肝组织中TGF-β,ALR的含量,抑制纤维结缔组织的增生。Objective:To study the molecular mechanism of treatment by Sanjia powder on the hepatic fibrosis in rats.Method: Hepatic fibrosis model of rat was established by administration of CCl4.Rats were divided into model group,malotilate group and low,middle,high dosage groups of Sanjia powder.After eight weeks,the level of transforming growth factor β(TGF-β),augmenter of liver regenration(ALR),biochemical and hepatic fibrosis pathology were observed for different groups.Result: The concentrations of HA,LN,PⅢNP,PⅣ in serum and transforming growth factor β,augmenter of liver regenration in liver of model group were higher than those in the control(P0.01).Compared with the model group,all the Sanjia powder dosage groups could improve the liver function,reduce serum markers of hepatic fibrosis(P0.05).Conclusion: Sanjia powder inhibited rat hepatic fibrosis induced by CCl4,and the mechanism is likely related to decrease of the expression of TGF-β and ALR.
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