芪归银对铜绿假单胞菌致肺炎大鼠免疫调节作用初探

Preliminary Study on the Immunomodulatory Effect of Qiguiyin on Pseudomonas Aeruginosa-induced Pneumonia in Rats

目的:初步探索芪归银对耐药铜绿假单胞菌(PA)致肺炎大鼠的免疫影响,为全面揭示其疗效机制奠定基础。方法:在空白和模型对照基础上,设置芪归银实验组与阿莫西林西药干预对照组。采集各组肺组织,并腹主动脉采血分离血清。检测肺组织中高迁移率族蛋白B1(HMGB1)的蛋白表达,血清中白细胞介素1β(IL-1β)和肿瘤坏死因子α(TNF-α)的浓度,进一步深入检测肺组织中HMGB1及其受体晚期糖基化终末产物受体(RAGE)、Toll-样受体4(TLR4)的基因表达。结果:模型组大鼠肺组织HMGB1蛋白及基因表达较对照组均明显升高,芪归银可一定程度降低其蛋白和基因表达;但阿莫西林对HMGB1和受体RAGE、TLR4的基因表达影响更为显著。模型组大鼠血清中IL-1β和TNF-α浓度较对照组均明显升高,芪归银可降低二者浓度,其中,对TNF-α浓度影响较阿莫西林更为显著。结论:肺炎发生时,芪归银对肌体核心免疫网络因子HMGB1及其受体RAGE、TLR4表达均有影响,对重要信号通路效应分子IL-1β和TNF-α也有影响,更深入的疗效机制有待进一步研究揭示。

Objective: To explore the immune effects of Qiguiyin on the rats with pneumonia induced by drug-resistant Pseudomonas aeruginosa (PA) and lay a foundation for revealing the therapeutic mechanism of Qiguiyin. Methods: On the basis of blank and model control, Qiguiyin experimental group and Amoxicillin western medicine intervention control group were set up.Pulmonary tissue was collected from each group,and abdominal aorta blood was collected to separate serum.Detect the expression of high mobility group protein B1 (HMGB1) in lung tissue,the concentration of interleukin-1β(IL-1β) and tumor necrosis factor-α(TNF-α) in serum, and further detect the gene expression of HMGB1 and its receptors, receptors for advanced glycation end products (RAGE) and Toll-like receptor 4 (TLR4) in lung tissue.Results: The expression of HMGB1 protein and gene in lung tissue of model group was significantly higher than that of control group. Qiguiyin could reduce the expression of HMGB1 protein and gene to a certain extent, but amoxicillin had more significant effect on the expression of HMGB1 and receptors RAGE and TLR4.The concentration of IL-1β and TNF-α in serum of model group was significantly higher than that of control group. Qiguiyin could decrease the concentration of IL-1β and TNF-α,especially the effect of amoxicillin on TNF-α was more significant.Conclusion: When pneumonia occurs, Qiguiyin has an effect on the expression of HMGB1 and its receptors RAGE and TLR4, as well as on the important signaling pathway effectors IL-1β and TNF-α.Further study is needed to reveal the mechanism of therapeutic effect.