Baicalin inhibit Mycobacterium tuberculosis in vivo by regulating the expression of Toll like receptor 4 and nuclear factor κB / 预防医学

ABSTRACT

Objective@#To study the mechanism of baicalin in inhibiting Mycobacterium tuberculosis（MTB）and to provide reference for drug-resistant tuberculosis treatment.@*Methods@#Forty male Kunming mice were injected isoniazid-resistant MTB into their tail veins to build models of infection. They were evenly divided into MTB group,isophosiazone group,NF-κB inhibition group and baicalicin group according to treatment. The lung tissue and peripheral blood of the mice were collected on the 8th day after modeling. The morphological changes of the lungs were observed by HE staining. The number of MTB in lung tissue was detected by acid-fast staining and quantitative PCR. The number of macrophagein lung tissue was detected by immunohistochemistry. The expression of NF-κB and TLR4 in monocytes/macrophages were detected by flow cytometry. @*Results@#The average weight of mice in the baicalicin group was significantly higher than that in the MTB group,the isophosiazone group and the NF-κBinhibition group（P<0.05）. The average fluorescence intensity of NF-κB and TLR4 in monocytes/macrophages in the baicalicin group were 448.21±30.61 and 401.01±34.58,which were significantly higher than those in the MTB group and the isophosiazone group（P<0.05）. Typical tuberculous chronic granulomatous lesions were observed in the MTB group,isophosiazone group and NF-κB inhibition group,except the baicalin group. The mean number of MTB and CD68+ macrophagesin lung tissue of mice in the baicalin group were significantly less than that in the MTB group,the isophosiazone group and the NF-κB inhibition group（P<0.05）. @*Conclusion@#Baicalin achieves an anti-tuberculosis effect by regulating the expression of NF-κB and TLR4 in macrophages,which can be weakened by adding NF-κB inhibitor.