藏药郎庆阿塔对肝纤维化大鼠胶原代谢的影响  

Effect of Langqing Ata on Metabolism of Collagen in Rat Hepatic Fibrosis Model

作　　者：薛娟[1,2] 彭蕴茹[2] 丁永芳[2] 黄一平[2] 王新敏[3] 

机构地区：[1]江苏大学药学院,江苏镇江212013 [2]江苏省中医药研究院,南京210028 [3]南京中医药大学江苏省方剂高技术研究重点实验室,南京210046

出　　处：《中国实验方剂学杂志》2012年第24期260-265,共6页Chinese Journal of Experimental Traditional Medical Formulae

摘　　要：目的:观察藏药郎庆阿塔对肝纤维化大鼠胶原代谢的影响。方法:采用复合因素(皮下注射40%CCl4/橄榄油溶液+高脂低蛋白复合饲料喂养+给予5%乙醇饮水)构建大鼠肝纤维化模型,造模6周后,于第7周开始分组给药,设置正常对照组、模型组、阳性药组[复方鳖甲软肝片(0.55 g.kg-1]、郎庆阿塔高、中、低剂量组(按生药量计为11.4,5.7,2.85 g.kg-1),分别ig给药7周。实验末期,取肝组织,HE染色观察肝脏组织的病理学变化,Masson染色观察肝组织内纤维化程度,免疫组化法检测肝组织中金属蛋白酶组织抑制因子I(TIMP-I)的表达水平,荧光定量PCR(RTFQ PCR)法测定药物对肝纤维化大鼠肝组织中I型胶原蛋白(CoL-I)mRNA表达的影响。结果:郎庆阿塔高、中剂量对肝纤维化大鼠肝纤维组织增生、肝组织炎症活动度均有显著的改善作用(P<0.05),免疫组化结果表明,郎庆阿塔能明显降低肝纤维化大鼠肝组织中TIMP-I的表达水平(P<0.01),高剂量组阳性率(4.80±0.92)与模型组(8.60±1.52)相比显著下降;此外,郎庆阿塔还能剂量依赖性地降低CoL-I mRNA表达水平,其中高剂量组与模型组相比较有显著性差异(P<0.01)。结论:郎庆阿塔能明显改善肝纤维组织增生,降低肝组织中TIMP-I和CoL-I mRNA的表达,发挥其抗肝纤维化作用。Objective： To observe the effect of Langqing Ata （LQAT） on the metabolism of collagen in rat hepatic fibrosis model. Method： Composite factors （subcutaneous injection of 40% CC14/olive oil solution ＋ high-fat and low-protein compound feed ＋ give 5% ethanol drinking water） were used to establish rat liver fibrosis model. Except the normal control group, the model rats were divided into five groups as model group, Fufang Biejia Ruangan table group （0.55 g ·kg^-1） and LQAT groups at three doses （11.4, 5.7, 2.85 g ·kg^-1 respectively）. The rats were orally treated with corresponding decoctions once a day for 7 weeks. At the end of the dosing cycle, rats were sacrificed and livers were collected and then were dyed by hematoxylin-eosin staining to observe the pathological changes. The degree of fibrosis in liver tissue was observed by Masson staining. The expression levels of tissue inhibitor of metal protease 1 （TIMP-I） in liver tissue were detected by immunohistochemistry method. The expression levels of type 1 collagen （CoL-I） mRNA in livers were measured by Real-time fluorescence quantitative PCR （RTFQ PCR）. Result： The fiber tissue proliferation and liver inflammation activity on the hepatic fibrosis could be ameliorated by the high and middle dose groups （P 〈 0.05-P 〈 0.01 ）. The immunohistochemical results showed that LQAT significantly reduced the expression levels of TIMP-I in livers （P 〈0.01 ）. Results also showed the dose-dependent inhibition of LQAT on the expression levels of CoL-I mRNA in livers, and the high dose group showed significant difference （P 〈 0.01 ） compared with the model group. Conclusion： LQAT played the role of anti-liver fibrosis by significantly improving hepatic fibrous tissue proliferation, and reducing the expression of TIMP-I and CoL-I mRNA.

关 键 词：郎庆阿塔 金属蛋白酶组织抑制因子I Ⅰ型胶原 荧光定量PCR 

分 类 号：R285.5[医药卫生—中药学]