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目的:探讨加味千金苇茎汤对慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)大鼠肺组织单免疫球蛋白IL-1相关蛋白(single immunoglobulin IL-1 related protein,SIGIRR)及其m RNA表达的影响。方法:Wistar雄性大鼠随机分为正常组、模型组、地塞米松组和加味千金苇茎汤组(每组8只)。采用脂多糖气管滴注联合烟熏方法建立COPD大鼠模型,采用免疫组化ABC法和实时荧光定量聚合酶链反应检测SIGIRR蛋白及其m RNA表达,观察加味小青龙汤对上述指标以及肺组织病理形态学变化的影响。结果:与正常组比较,模型组肺组织SIGIRR蛋白表达明显降低(P<0.05);与模型组比较,地塞米松组和加味千金苇茎汤组肺组织SIGIRR蛋白及其m RNA的表达明显升高(P<0.01)。病理观察显示,模型组肺内细支气管上皮空泡变性坏死脱落,管壁结构破坏,大量炎细胞浸润,腔内炎性充满渗出物,地塞米松组和加味千金苇茎汤组仅见轻度肺间质炎症。结论:加味千金苇茎汤能够减轻慢性阻塞性肺疾病模型大鼠肺组织的损伤,对COPD模型肺组织有保护作用,其机制可能与其能够上调SIGIRR蛋白表达有关。
Objective: To investigate the effect of Modified Qianjinwei Stem Decoction on the expression of single immunoglobulin IL-1 related protein (SIGIRR) and its m RNA in chronic obstructive pulmonary disease (COPD) The impact of expression. Methods: Male Wistar rats were randomly divided into normal group, model group, dexamethasone group and Jiawei Qianjinwei Soup Decoction group (n = 8). The model of COPD was established by intratracheal instillation of lipopolysaccharide combined with smoking, and the expression of SIGIRR protein and m RNA were detected by immunohistochemical ABC method and real-time fluorescence quantitative polymerase chain reaction. The effects of Modified Xiao Qinglong Decoction on the above indexes and lung tissue Impact of pathological changes. Results: Compared with normal group, the expression of SIGIRR protein in lung tissue of model group was significantly lower than that in normal group (P <0.05). Compared with model group, the expression of SIGIRR protein and m RNA in lung tissue of dexamethasone group and Jiawei Qianjinweishitang group were significantly increased High (P <0.01). Pathological observation showed that the model group, the bronchial epithelial cell vacuolar degeneration and necrosis, the destruction of the wall structure, a large number of inflammatory cell infiltration, intraluminal inflammatory exudate, dexamethasone group and Jiawei reed stem soup group only mild Interstitial inflammation. Conclusion: Modified Qianjinwei Stem Decoction can reduce lung injury in COPD model rats and protect the lung tissue of COPD model. The mechanism may be related to the increase of SIGIRR protein expression.