CAJ | 학술논문

目的：观察川芎嗪对四氯化碳诱导的肝纤维化大鼠肝组织Nrf2/ARE信号通路的影响,探讨川芎嗪治疗肝纤维化的作用机制。方法四氯化碳皮下注射制备大鼠肝纤维化模型,设立正常对照组、肝纤维化模型组和川芎嗪治疗组,川芎嗪治疗组在造模过程中每天给予盐酸川芎嗪注射液腹腔注射,6周后,乙醚麻醉,腹主动脉采血,产色基质偶氮法鲎试剂定量测定血浆内毒素；肝组织常规HE染色观察肝脏病变,天狼猩红胶原染色、肝组织羟脯氨酸含量测定评测肝纤维化程度；West-blotting法检测肝组织内Nrf2蛋白的表达, TBA法检测肝组织丙二醛(MDA)水平,酶显色定量分析法检测肝组织谷胱甘肽-S-转移酶(GST)含量。结果川芎嗪治疗组与肝纤维化模型组相比,肝损伤较轻,肝纤维化程度明显降低,血浆内毒素含量降低, Nrf2蛋白表达量增多,肝组织中MDA含量降低, GST的含量升高。结论川芎嗪的抗肝纤维化作用可能与其降低内毒素血症,激活肝内Nrf2/ARE抗氧化通路进而使得抗氧化酶GST等含量增加有关。
목적：관찰천궁진대사록화탄유도적간섬유화대서간조직Nrf2/ARE신호통로적영향,탐토천궁진치료간섬유화적작용궤제。방법사록화탄피하주사제비대서간섬유화모형,설립정상대조조、간섬유화모형조화천궁진치료조,천궁진치료조재조모과정중매천급여염산천궁진주사액복강주사,6주후,을미마취,복주동맥채혈,산색기질우담법후시제정량측정혈장내독소；간조직상규HE염색관찰간장병변,천랑성홍효원염색、간조직간포안산함량측정평측간섬유화정도；West-blotting법검측간조직내Nrf2단백적표체, TBA법검측간조직병이철(MDA)수평,매현색정량분석법검측간조직곡광감태-S-전이매(GST)함량。결과천궁진치료조여간섬유화모형조상비,간손상교경,간섬유화정도명현강저,혈장내독소함량강저, Nrf2단백표체량증다,간조직중MDA함량강저, GST적함량승고。결론천궁진적항간섬유화작용가능여기강저내독소혈증,격활간내Nrf2/ARE항양화통로진이사득항양화매GST등함량증가유관。
Objective To explore the effect of ligustrazine on Nrf2/ARE pathway in liver tissue of hepatic fibrosis rats induced by CCl4 for studying the mechanism of its effect on hepatic fibrosis. Methods Hepatic fibrosis in rats was induced by carbon tetrachloride, rats were randomly divided into normal control group, hepatic fibrosis group and treatment group. treatment group rats were given ligustrazine intraperitoneally everyday while inducing hepatic fibrosis by carbon tetrachloride. After 6 weeks, rats were killed for collecting blood and liver tissues. Endotoxin in blood plasma was measured with a limulus amebocyte lysate test kit. The pathological changes of liver were observed by hematoxylin-eosin staining, the degree of liver fibrosis was assessed by stained of Sirius red for collgen and the contents of hydroxyproline in liver tissues. Nrf2 protein expression in liver tissues was detected by West-blotting method. The contents of malondialdehyde(MDA) in liver tissues were determined by TBA method, glutathione S-transferase(GST) by colorimetric enzymatic assay. Results Fibrotic changes in liver of treatment group were ameliorated significantly compared with the hepatic fibrosis model group, and the content of plasma endotoxin were reduced, liver expression of Nrf2 was increased as well as GST, MDA was reduced accordingly. Conclusion The protective effect of ligustrazine on liver fibrosis is possibly related to reducing endotoximia and activating Nrf2/ARE pathway in liver, thus increasing the content of antioxidant enzymes such as GST.