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出 处:《海南医学》2012年第18期15-17,共3页Hainan Medical Journal
摘 要:目的探讨赖诺普利对胆汁淤积性肝硬化的抗肝纤维化作用。方法采用胆总管结扎术制备大鼠胆汁淤积性肝硬化模型,分为赖诺普利组和模型对照组。前者于术后第3周给药,具体为:赖诺普利0.1mg/kg灌胃,1次/d,连续4周;后者于术后第3周给予生理盐水10ml/kg灌胃,1次/d,连续4周。同期设假手术组作为空白对照。6周后处死大鼠,取三组实验大鼠肝组织进行常规病理染色和胶原纤维染色;用放射免疫法测定各组血清透明质酸酶(HA)和层粘连蛋白(LN)含量,并测定肝组织羟脯氨酸(HYP)含量。结果与空白对照组比较,赖诺普利组和模型对照组的血清HA、LN活性均下降,而肝组织HYP含量均升高,差异均有统计学意义(P<0.05)。与模型对照组比较,赖诺普利组肝细胞损伤和肝纤维化程度较轻。赖诺普利组的血清HA、LN活性以及肝组织HYP含量分别为(62.1±2.23)ng/ml、(42.8±6.23)ng/ml和(1.6±0.15)μg/mg,明显低于模型对照组的(97.5±4.50)ng/ml、(66.5±7.32)ng/ml和(2.0±0.27)μg/mg(P<0.05)。结论赖诺普利可以有效改善胆汁淤积性肝硬化大鼠模型的肝纤维化程度。Objective To study the effect of lisinopril on bile duct ligation-induced biliary cholestasis on liver of mice. Methods The experimental model mice of hepatic fibrosis was induced by common bile duct ligation, which were divided into model control group and lisinopril group. Three weeks after the operation, lisinopril (0. 1 mg/kg) and physiological saline (10 ml/kg) were administrated respectively by intragastric in lisinopril group and model control group, with once a day for 4 consecutive weeks. False operation group was as blank control in the same period. All the mice were sacrificed six weeks later. Liver tissues of the three groups were detected by routine histological staining and collagen fiber staining; serum hyaluronate lyase (HA) and laminin (LN) levels were measured by radioimmu- noassay, including liver hydroxyproline (HYP) content. Results Serum HA and LN contents in model control group and lisinopril group were decresed and liver HYP content were increased compared with those in blank control group (P〈0.05). Liver ceils injury and the degree of liver fibrosis in lisinopril group were lighter compared with those in mod- el group. Serum HA, LN contents and liver HYP content in lisinopril group were (62.1±2.23) ng/ml, (42.8±6.23) ng/ml and (1.6±0.150) μg/mg, significantly lower than those in model group [(97.5±4.50)ng/ml, (66.5±7.32) ng/ml and (2.0± 0.27) μg/mg; all the 〈0.05]. Conclusion Lisinopril has effect on preventing hepatic fibrosis in mice model with bile duct ligation-induced biliary cholestasis.
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