参麦注射液及氨茶碱对肺气肿大鼠小气道平滑肌细胞凋亡及相关基因表达的影响

作者	单位
牛汝楫	华中科技大学同济医学院附属同济医院呼吸内科武汉430030
傅娟	华中科技大学同济医学院附属同济医院呼吸内科武汉430030
刘辉国	华中科技大学同济医学院附属同济医院呼吸内科武汉430030

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中文摘要:

目的 :探讨参麦注射液及氨茶碱对木瓜蛋白酶致大鼠肺气肿小气道平滑肌细胞凋亡及其Fas/FasL系统表达的影响。方法 :采用免疫组织化学及TUNEL法 ,检测气管内注入木瓜蛋白酶后肺气肿模型 1、3、5、7、15、30天组和正常对照组 ,小气道平滑肌细胞凋亡及其Fas/FasL系统表达 ,以及参麦注射液和氨茶碱对其影响。结果 :正常对照组小气道平滑肌细胞Fas、FasL表达很低 ,阳性率分别为 (2 31±0 5 5 ) %、(1 2 8± 0 4 7) % ,气道内注入木瓜蛋白酶后 ,空白组小气道平滑肌细胞 (SASMC)Fas、FasL表达随着注酶时间的延长而阳性率也明显增加 ,参麦注射液有抑制大鼠SASMCFas、FasL表达的作用 ,而氨茶碱作用不明显。同时 ,发现正常对照组大鼠SASMC凋亡百分率也很低 (0 87± 0 32 ) % ,气道内注入木瓜蛋白酶后 ,空白组SASMC凋亡百分率随着注酶时间的延长而凋亡百分率也明显增加 ,用参麦注射液治疗后可使大鼠SASMC凋亡降低 ,而氨茶碱作用不明显。结论 :在肺气肿形成过程中 ,Fas和FasL参与了小气道平滑肌细胞的凋亡调控 ,参麦注射液可能通过抑制炎性介质释放 ,影响Fas和FasL蛋白表达和减少小气道平滑肌细胞的凋亡 ,对肺气肿有一定的治疗作用

英文摘要:

To investigate the effect of Shenmai Injectio n (SMI) and aminophylline on small airway smooth muscle cell (SASMC) apoptosis and the Fas/FasL expression in the papain induced emphysema model rats. Methods: Emphysema model in rat was established by a single in tratracheal instillation of papain. Apoptosis and Fas/FasL expression of SASMC w ere examined by immunohistochemical SABC and TUNEL assay at 1, 3, 5, 7, 15 and 3 0 days after modelling, and the effect of SMI and aminophylline on them were obs erved. Results: Fas, FasL expressions in normal SASMC were very low w ith a positive rate of (2.31±0.05)% and (1.28±0.47)% respectively. After papai n inst illation, the positive rates increased along with the prolonging of instillation time . SMI showed an inhibition on SASMC Fas and FasL expression but aminophylline di dn′t show. SASMC apoptosis was very low in normal rats with a rate of (0.87±0. 32)%, it also raised after papain instillation and increased progressively along with th e instillation time. SMI treatment could lower the apoptosis rate but aminophyll ine couldn′t. Conclusion: Fas and FasL participated the SASMC apoptosis modu lation in emphysema formation. SMI shows a definite treatment effect on emphysem a by influencing the Fas and FasL protein expression and reducing SASMC apoptosi s through inhibiting the release of inflammatory mediator.

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