Effect of Modified Yangyin Qingfei Decoction(养阴清肺汤加味)on Inflammation in Mice Infected with Mycoplasma Pneumoniae and TLR-2/MyD88/NF-κB Signaling Pathway
Objective To investigate the effect of Modified Yangyin Qingfei Decoction(养阴清肺汤加味,YQDP)on the in-flammatory response and Toll-like receptor 2(TLR-2)/myeloid differentiation factor 88(MyD88)/nuclear factor-κB(NF-κB)signaling pathwayin in mice infected with mycoplasma pneumoniae(MP).Methods B ALB/c mice(n=60)were randomly divided into normal group,MP model group,azithromycin group,and low,medium and high dose groups of YQDP,models of MP infection were established except for the normal group.After successful modeling,all mice were treated for 7 days.The lung tis-sue and serum of mice was collected at the last administration.The lung pathological changes of lung tissue were observed by HE staining,the levels of interleukin-6(IL-6),interleukin-8(IL-8)and interleukin-17(IL-17)in serum were detected by ELISA,TLR-2,MyD88 and NF-κB mRNA and protein expression levels were detected by RT-PCR and Western blot.Results Compared with those of the normal group,the lung tissue of the model group was less intact,the most of the alveolar structures were seriously damaged,the alveolar septum was significantly thickened,and a large number of inflammatory cells were visible.The contents of IL-6,1L-8 and IL-17 in serum were significantly increased(P＜0.05).The expressions of TLR-2,MyD88,NF-κB mRNA and protein in lung tissues were increased(P＜0.05).Compared with those of the model group,after treatment,lung histopathology showed that the alveolar structure was significantly restored,and the inflammatory cell infiltration around the alveoli was reduced to varying degrees.The contents of IL-6,IL-8 and IL-17 in serum were significantly reduced(P＜0.05).The expressions of TLR-2,MyD88,NF-κB mRNA and protein in lung tissues were decreased(P＜0.05).The reduc-tion trend of YQDP treatment group was dependent on its low,medium and high doses.Conclusions YQDP may reduce lung in-flammation in MP-infected mice by regulating the TLR-2/MyD88/NF-κB signaling pathway.
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