【摘要】 目的探讨清金化痰汤调节慢性阻塞性肺疾病(COPD)模型大鼠气道黏液高分泌的作用机制。方法 Wistar大鼠随机分为正常组、模型组、清金化痰汤组与克拉霉素组,每组10只。除正常组外,其余3组均采用气管内注入脂多糖和烟熏复合法建立COPD模型,分别给予生理盐水、清金化痰汤、克拉霉素灌胃,连续30 d。实验第31日,处死大鼠提取肺组织,每组随机选取6只,采用实时荧光定量PCR检测肺组织中性粒细胞弹性蛋白酶(NE)、表皮生长因子(EGFR)、黏蛋白5AC(MUC5AC)基因表达。结果模型组大鼠肺组织NE、MUC5AC m RNA表达较正常组升高;与模型组比较,清金化痰汤组、克拉霉素组NE、MUC5AC m RNA表达均显著降低,清金化痰汤组NE、MUC5AC m RNA表达较克拉霉素组显著降低;清金化痰汤组EGFR m RNA表达较模型组显著降低。结论清金化痰汤通过调节NE/EGFR/MUC5AC信号转导通路,抑制气道黏液高分泌。更多还原

【Abstract】 Objective To investigate the action mechanism of Qingjin Huatan Decoction on regulating COPD rats with mucus hypersecretion in airway. Methods Fifty 6-8 week old Wistar male rats were randomly divided into healthy group, model group, Qingjin Huatan Decoction group, clarithromycin group, 10 rats in each group. Except for healthy group, all the other groups were used the combination method of injecting LPS and smudging to establish COPD models. The last three groups were fed with normal saline, Qingjin Huatan Decoction, clarithromycin respectively for 30 days. On the 31 st day of the experiment, the rats were put to death to take lung tissue. 6 rats from each group were chosen randomly, and the protein expressions of NE, EGFR and MUC5 AC m RNA in lung tissue were detected by real-time fluorescent quantitative PCR. Results The expressions of NE, MUC5 AC m RNA in lung tissue of COPD rats were higher than the healthy group. Compared with model group, the expressions of NE m RNA and MUC5 AC m RNA in Qingjin Huatan Decoction group and clarithromycin group were markedly lower, while the expressions of NE, MUC5 AC m RNA in Qingjin Huatan Decoction group were significantly lower than those in clarithromycin group. The expression of EGFR m RNA in Qingjin Huatan Decoction group was lower than that in model group. Conclusion Qingjin Huatan Decoction can inhibit mucus hypersecretion in airway through NE/EGFR/MUC5 AC signal transduction pathway.更多还原