哮喘平对哮喘模型大鼠肺组织细胞凋亡相关调控基因蛋白Bcl-2、Bax水平的影响

目的:观察哮喘平对哮喘大鼠模型肺组织细胞凋亡相关调控基因蛋白Bcl-2、Bax水平的影响,研究哮喘平治疗哮喘的作用机制。方法:将60只SD雄性大鼠随机分为6组,每组10只,即空白对照组、哮喘模型组、桂龙咳喘宁组、哮喘平低剂量组、哮喘平中剂量组、哮喘平高剂量组。以卵蛋白致敏复制大鼠哮喘模型,成功复制模型21 d后,空白对照组和模型组每天给予等量的氯化钠溶液灌胃,连续给药2周后处死大鼠,解剖大鼠并取出肺组织。采用免疫组化法测定大鼠肺组织中细胞凋亡相关调控基因蛋白Bcl-2及Bax的表达。结果:与空白对照组比较,模型组大鼠Bcl-2表达升高,Bax表达降低(P0.01),与模型组比较,给药组大鼠Bcl-2表达降低,Bax表达升高(P0.05,P0.01);与桂龙咳喘宁组比较,哮喘平中高剂量组Bcl-2表达显著降低,Bax表达显著升高(P0.01)。结论:哮喘平可以降低抑凋亡基因蛋白Bcl-2的表达,升高促凋亡基因蛋白Bax的表达。

Effect of Xiaochuanping on Levels of Regulatory Genes Bcl-2 and Bax Related to Apoptosis in Lung Tissue of Asthmatic Rats

Objective:To study the effect of Xiaochuanping on the levels of regulatory genes Bcl-2 and Bax related to apoptosis in lung tissue of asthmatic rats. Methods:Sixty SD male rats were randomly divided into 6 groups,with 10 rats in each group,namely blank control group,asthma model group,Guilong Kechuanning group,low-dose Xiaochuanping group,middle-dose Xiaochuanping group and high-dose Xiaochuanping group. The asthma model rats were induced by ovalbumin. After 21 days of successful replication,each treatment group began to administer drugs. The blank control group and the model group were given the same amount of sodium chloride solution every day.After 2 weeks of administration,rats were dissected and the lung tissue was taken out. Immunohistochemical method was used to detect the expression of regulatory genes Bcl-2 and Bax related to apoptosis in rat lung tissue. Results:Compared with the blank control group,the expression of Bcl-2 increased and the expression of Bax decreased in the model group(P< 0.01). Compared with the model group,the expression of Bcl-2 decreased and the expression of Bax increased in the medication group(P< 0.05,P< 0.01). Compared with Guilong Kechuanning group,the expression of Bcl-2 significantly decreased and the expression of Bax significantly increased(P< 0.01) in the middle-dose and high-dose Xiaochuanping groups. Conclusion:Xiaochuanping can reduce the expression of anti-apoptotic gene protein Bcl-2 and increase the expression of pro-apoptotic gene protein Bax.