清化瘀毒方对酒精性肝纤维化模型大鼠的TLR4-MyD88-NF-κB信号通路影响  

The impact of QHYD formula on TLR4-MyD88-NF-κB signaling pathway in alcoholic liver fibrosis model rats

作　　者：张斌 王培劼 丁静 何国浓 毛飞寅 魏冬梅 王玲玲 卞尧尧[2] 王邦才 ZHANG Bin;WANG Peijie;DING Jing;HE Guonong;MAN Feiyin;WEI Dongmei;WANG Lingling;BIAN Yaoyao;WANG Bangca(Department of Gastroenterology,Ningbo Municipal Hospital of Traditional Chinese Medicine,Ningbo 315010,China;School of Nursing,Nanjing University of Chinese Medicine,Nanjing 210023,China)

机构地区：[1]宁波市中医院消化科,315010 [2]南京中医药大学护理学院,210046

出　　处：《免疫学杂志》2018年第11期952-956,共5页Immunological Journal

基　　金：浙江省名老中医专家传承工作室建设计划(GZS2017018);宁波市自然基金(2015A610186)

摘　　要：目的探讨清化瘀毒方干预酒精性肝纤维化大鼠的可能作用机制。方法将50只SD大鼠随机分为:空白(正常)对照组、模型对照组、清化瘀毒方低、中、高剂量干预组(每组各10只)。造模成功后,对照组以等量生理盐水灌胃,每只2 ml/d。清化瘀毒方低、中、高剂量组分别以50、100、200 mg/(kg·d)灌胃,连续12周。免疫荧光法检测TLR4治疗干预后的表达。Western blot方法检测各组NF-κB与TLR4/MyD88蛋白表达。结果与空白组对比各组TLR4免疫荧光表达强度增强,清化瘀毒方低、中、高剂量干预组较模型组明显减少。模型组TLR4、MyD88和NF-κB表达升高,与空白组比较有显著性差异(P<0.01)。与模型组比较,清化瘀毒方高剂量组TLR4、MyD88和NF-κB表达有显著性差异(P<0.01)。与模型组比较,清化瘀毒方中剂量组NF-κB表达有显著性差异(P<0.01)。结论清化瘀毒方治疗酒精轻肝纤维化的作用机制可能与调控TLR4、MyD88、NF-κB及TLR4-MyD88-NF-κB信号通路有关。To evaluate the effects of QHYD Formula on alcoholic liver fibrosis, SD rats were recruited and randomly divided into the normal group, model group, QHYD formula low-dose group, QHYD formula middle-dose group, and QHYD formula high-dose group, with 10 rats in each group. Rat model of alcoholic liver fibrosis was constructed by complex factors dominated as alcohol for 12 weeks. Both the normal and model groups were gavaged with 2 ml/d normal saline respectively, while the QHYD formula low-dose group, QHYD formula middle-dose group and the QHYD high dose group were gavaged with QHYD of 50 mg/（kg·d）, 100 mg/（kg·d） and 200 mg/（kg·d）,respectively. Immunofluorescence assay was used to detect the expression of TLR4 after intervention; the protein expression of NF-κB and TLR4/MyD88 were detected by Western blotting. Data showed that the immunofluorescence expression intensity of TLR4 was enhanced in model group compared with normal rat, and was significantly reduced in QHYD formula low-dose, middle-dose and high dose groups compared with the model group. TLR4, MyD88 and NF-κB expression increasedin the model group, as compared with the blank group（P〈0.01）; QHYD formula at high-dose significantlydown-regulated the expressions of TLR4, MyD88 and NF-κB（P〈0.01）, while QHYD formula at middle-dosesignificantly down-regulated the expression of NF-κB （P〈0.01）. Taken together, the possible mechanism of QHYD formula for alcoholic liver fibrosis may related to the inhibition of cell proliferation and regulation of the TLR4, MyD88, NF-κB and TLR4-MyD88-NF-κB signaling pathway

关 键 词：酒精性肝纤维化 清化瘀毒方 酒精肝 TOLL样受体 髓样分化因子 

分 类 号：R392.5[医药卫生—免疫学]