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目的探讨补肾益肺消癥方干预特发性肺纤维化大鼠含半胱氨酸的天冬氨酸蛋白水解酶(Caspase)-12信号通路关键分子基因和蛋白表达的作用机制。方法以博莱霉素造大鼠肺纤维化模型。吡非尼酮作为阳性对照药物,补肾益肺消癥方分别于造模中(预防组)、造模后(治疗组)及实验全程(防治组)进行干预。Masson染色观察大鼠病变肺组织纤维化改变的程度,Western blot、Real-time PCR检测病变肺组织中Caspase-12信号通路相关分子基因与蛋白表达的改变。结果阳性对照组和中药各组肺泡结构轻度改变,有少量胶原纤维沉积,纤维化程度较模型组明显改善。模型组大鼠肺组织中Caspase-12通路基因及蛋白表达比正常组明显升高(P<0.05),阳性组及中药各组Caspase-12通路基因及蛋白表达较模型组明显降低(P<0.05或P<0.01),其中中药防治组效果更优。结论补肾益肺消癥方可以通过干预Caspase-12通路关键分子的表达,调控肺泡上皮细胞内质网应激反应,延缓和抑制特发性肺纤维化病理改变进程。
Objective To investigate the mechanism of Bushen Yifei Xiaozheng Fang intervening in key gene and protein expression of cysteine-containing caspase-12 signaling pathway in idiopathic pulmonary fibrosis rats. Methods Pulmonary fibrosis was induced by bleomycin in rats. Pirfenidone as a positive control drug, Bushen Yifei Xiao Fang were in the modeling (prevention group), modeling (treatment group) and the whole experiment (prevention group) intervention. Masson staining was used to observe the degree of pulmonary fibrosis in rats. Western blot and Real-time PCR were used to detect the expression of Caspase-12 signaling pathway in lung tissue. Results The alveolar structure of the positive control group and the traditional Chinese medicine group changed slightly with a small amount of collagen deposition and the degree of fibrosis was significantly improved compared with the model group. The expression of Caspase-12 pathway gene and protein in lung tissue of model group was significantly higher than that of normal group (P <0.05), while the expression of Caspase-12 pathway gene and protein in positive group and TCM group was significantly lower than that of model group (P <0.05 Or P <0.01), of which Chinese medicine prevention and treatment group is better. Conclusion Bushen Yifei Xiaozheng Recipe can inhibit the process of pathological changes of idiopathic pulmonary fibrosis by regulating the expression of key molecules of Caspase-12 pathway, regulating the endoplasmic reticulum stress response of alveolar epithelial cells.