Objective:Investigate the receptor proteinã€cytokine and miRNA levels in INH-resistant pulmonary tuberculosis mice infected with Chinese Compound Feilaokang (FLK), based on immune-inflammatory mechanisms to preliminary explore the effect of FLK to drug-resistant tuberculosis.Methods:Establishing the animal models of INH-resistant pulmonary tuberculosis through tail mainline,the mice were randomly divided into the following groups: group of INH-resistant bacterial strain (model group),group of INH,group of FLK, group of INH and FLK,and a blank group.The normal salineã€INHã€FLK were given separately for 56 days.â‘ To compare with the signs and avoirdupois of the mice in different groups.Bacterial cultivation of lung tissue were used after 4 weeks when the animal models were established.Observing the pathological changes of lung tissue, liver tissue and spleen tissue at the end of treatment.â‘¡Examining the expression of TLR2ã€TLR4ã€IL2 in lung tissue by immunohistochemical staining.â‘¢Examining the expression of miRNA-155 in lung tissue by real-time PCR.Result:â‘ Compared with the blank group,the weight change of model group had significant difference (P<0.05), colony on L-J culture medium were obvious. Compared with the model group, FLK could rise the mice weight normally (P<0.05), and alleviated the inflammation of the lungã€ã€liver and spleen tissue (P<0.05) â‘¡Compared with the blank group,expression of TLR2ã€TLR4 and miRNA-155 were rised observably in model group (P<0.05), while IL2 was obviously decreased(P<0.05).Compared with the model group,FLK had obvious inhibitory effect on the overexpression of TLRã€TLR4 and miRNA-155 (P<0.05),and increased contents of IL2 (P<.05).Conclusion:â‘ The method of establishing mice pulmonary tuberculosis model was successful through caudal vein while judgment and analysis based on generally signs〠objective indicators and stabilization of models.â‘¡FLK had the effects on improving the signs and tissue lesions, alleviating inflammatory reactions,inducing the overexpression of TLR2ã€TLR4 and miRNA-155 and increasing contents of IL2.â‘¢Animal infected mycobacterium tuberculosis led to high expression of TLR2ã€TLR4 and miRAN-155,perhaps the therapeutic mechanism is that FLK can interdict stimulation of some relative inflammation signal pathway, reduce experssion of inflammatory genes, dampen the inflammatory through the effect on inducing the level of TLR2ã€TLR4 and miRNA-155,besides FLK could rise the contents of IL2 to enhance immunity and alleviate the pathological damage caused by pulmonary tuberculosis,strengthen immune reaction to help fight infection. |