摘要
目的研究利福昔明对LPS-TLR4(Toll样受体4)通路的作用,以此来分析利福昔明抗肝衰竭后继发肝硬化的分子机制。方法选取就诊于我院肝内科住院患者共90例,分为3组,慢性肝炎组(n=30),肝衰竭组(n=30),肝衰竭药物治疗组(n=30)。Elisa检测血清中FN浓度、ET水平,HE染色观察各组肝脏结构的改变,用定量实时PCR(q-PCR)和Western Blot检测LPS-TLR4通路上关键分子TLR4和MyD88 mRNA和蛋白表达水平。结果肝衰竭药物组FN浓度、ET水平均较肝衰竭组明显下降,TLR4和MyD88 mRNA及蛋白表达水平均较肝衰竭组明显下降,差异均有统计学意义(P<0.05),药物治疗组肝组织结构病理变化较肝衰竭组减轻。结论利福昔明通过抑制LPS-TLR4信号通路,可能是缓解肝衰竭后继发肝硬化的作用机制之一。
OBJECTIVE To study the effect of rifaximin on LPS-TLR4 pathway,so as to analyze the molecular mechanism of rifaximin against liver cirrhosis after liver failure.METHODS A total of 90 patients hospitalized in the department of liver medicine of our hospital were selected and divided into three groups:chronic hepatitis group(n=30),liver failure group(n=30),and drug treatment group(n=30).Elisa detected the level of FN and ET in the serum of human,and HE staining observed the changes in the liver structure in each group.Real-time Quantitative PCR(q-PCR)and Western Blot were used to detect the mRNA and protein expression levels of TLR4 and MyD88,the key molecules on the LPS-TLR4 pathway.RESULTS The level of FN,ET,TLR4 and MyD88 mRNA and protein in the drug treatment group were significantly lower than those in the liver failure group,with statistically significant differences(P<0.05).The pathological changes of liver tissue structure in the drug treatment group were less than those in the liver failure group.CONCLUSION Rifaximin may be one of the mechanisms of relieving liver cirrhosis after liver failure by inhibiting the activity of LPS-TLR4 signaling pathway.
作者
刘晓燕
王艳丽
朱金照
郑磊
肖秀丽
LIU Xiao-yan;WANG Yan-li;ZHU Jin-zhao;ZHENG Lei;XIAO Xiu-li(Department of Gastroenterology,Mengchao Hepatobiliary Hospital of Fujian Medical University,Fuzhou 350025,China)
出处
《海峡药学》
2023年第5期72-76,共5页
Strait Pharmaceutical Journal
基金
福州市科技局基金(2021-S-097)。
