益气养阴方对肺间质纤维化大鼠肺组织TNF-α、TGF-β1和IFN-γ mRNA水平的影响

Effects of Yiqiyangyin recipe on the mRNA levels of TNF-α,TGF-β1 and IFN-γ of lungs in rats with pulmonary interstitial fibrosis

目的观察益气养阴方对大鼠肺间质纤维化模型肺组织形态结构及肿瘤坏死因子α(TNF-α)、转化生长因子β(TGF-β1)、γ干扰素(IFN-γ)mRNA水平的影响。方法通过气管内滴注博莱霉素建立大鼠肺间质纤维化模型后,随机分为正常组、模型组、中药组、醋酸泼尼松(激素)组、中药联合激素组。造模后第28天,开始灌胃给药,持续给药28 d后处死。分离出大鼠肺组织,行HE染色和Masson染色以观察形态学改变,原位杂交法检测肺组织中TNF-α、TGF-β1、IFN-γ的mRNA表达。结果模型组TNF-αmRNA、TGF-β1 mRNA阳性细胞率较其他4组明显升高,IFN-γmRNA阳性细胞率较其他4组降低;中药组与激素组、中药联合激素组相比,TNF-αmRNA阳性细胞率降低,IFN-γmRNA阳性细胞率略高;中药组TGF-β1 mRNA阳性细胞率略低于激素组。结论益气养阴方降低肺间质纤维化模型大鼠肺组织中TNF-α、TGF-β1的mRNA表达及增加肺组织内IFN-γmRNA的表达。

Objective To investigate the effects of Yiqiyangyin recipe on lung tissue morphological structure and mRNA levels of tumor necrosis factor α （TNF-α）, transforming growth factor beta-1 （TGF-β1） and interferon-y （IFN-y） in pulmonary interstitial fibrosis rat models. Methods The pulmonary interstitial fibrosis rat model was established by intrabronchial injection of bleomycin AS. After the model was set up, the rats were divided randomly into five groups, normal group, model group, prednisone acetate group, traditional Chinese medicine （TCM） group, and TCM plus prednisone acetate group. Twenty-eight days after modeling, all groups were subjected to gavage for another 28 days. Then the animals were executed in batch. Their lung tissues were separated and observed with HE staining and Masson staining. The mRNA levels of TNF-α, TGF-β1 and IFN-y were detected using in situ hybridization. Results The levels of TNF-α and TGF-β1 mRNAs were enhanced and IFN-γ mRNA was weakened in the model group as compared with the other groups at the same time points. Compared with the prednisone acetate group and the TCM plus prednisone acetate group, the expression of TNF-α mRNA was reduced and IFN-y mRNA was raised a little in the TCM group at the same time points. Compared with the prednisone acetate group at the same time points, the level of TGF-β1 mRNA decreased slightly in the TCM group. Conclusion Yiqiyangyin recipe could delay pulmonary fibrosis by reducing the mRNA levels of TNF-α and TGF-β1 and increasing IFN-γ mRNA in lung tissues of pulmonary intestitial fibrosis rats.