丹参、人参及蛤蚧组方对大鼠肺纤维化凋亡基因作用的研究

The effect of danshen,renshen and gejie compound medication on the apoptosis-related gene in IPF rats

目的研究丹参、人参及蛤蚧组方对博莱霉素致大鼠肺间质纤维化模型凋亡基因的表达,探讨该组方抗肺纤维化的作用机制。方法 SD雄性大鼠50只随机分为对照组、模型组、醋酸泼尼松组、治疗Ⅰ组(低剂量组:丹参83 mg/kg、人参50mg/kg及蛤蚧50 mg/kg)及治疗Ⅱ组(高剂量组:丹参166 mg/kg、人参50 mg/kg及蛤蚧50 mg/kg);于第28天处死大鼠,RT-PCR法检测大鼠肺组织bax及bcl-2基因mRNA表达水平,用单克隆抗体免疫组化法检测bax及bcl-2蛋白含量。结果 bax基因mRNA及蛋白在模型组、醋酸泼尼松组、治疗Ⅰ组及治疗Ⅱ组的表达明显升高,与对照组相比差异有统计学意义(P<0.05);同时模型组升高幅度明显,治疗Ⅱ组升高幅度较低,两者相比差异有统计学意义(P<0.01);bcl-2基因mRNA及蛋白在醋酸泼尼松组、治疗Ⅰ组及治疗Ⅱ组的表达升高,并治疗Ⅱ组升高更明显,与模型组相比差异有统计学意义(P<0.05)。结论丹参、人参及蛤蚧组方能通过调节细胞凋亡,下调bax活性,增强Bcl-2的活性,抑制细胞凋亡,减少纤维积聚和纤维化形成。

Objective To observe the effect of danshen, renshen and Gejie compound medication on the apoptosis-Related Gene in IPF （ Idiopathic pulmonary interstitial fibrosis） rats caused by bleomycin. Methods Fifty SD rats in good conditions were divided into five groups at random ： control group, model group, prednisone group, therapeutic Ⅰ group, and therapeutic Ⅱ group. After administration with related dose of medicine, each group was sacrificed on 28 days. The mRNA of bax and bcl-2 were tested by RT-PCR, and the protein of bax and bcl-2 were determined by immunohistochemistry techniques. Results The mRNA and protein of bax in the model group, the prednisone group, and the two therapeutic groups were obviously higher than those of the control group （ P 〈 0. 05 ）. The model group showed more apparent increase whereas the therapeutic Ⅱ group＇s increase was less apparent （P 〈 0. 01 ）. However, The mRNA and protein of bcl-2 was higher in the model group, but in the prednisone group, the therapeutic Ⅰ group, and therapeutic group were obviously lower, especially in therapeutic Ⅱ group which had the lowest. Conclusion Danshen, renshen and gejie compound medication has obvious therapeutic effect through reducing fiber piling and restraining forming of fibrosis on rats lung with IPF caused by bleomycin, and it can regulate the expression of the apoptosis by inhibiting the bax expression, enhancing the bcl-2 expression and inhibiting the apoptosis of bronchial and alveolar epithelia cells.