摘要
目的观察一氧化氮(NO)供体硝普钠(SNP)是否诱导哮喘大鼠气道平滑肌细胞(ASMCs)凋亡。方法W istar大鼠10只,用卵白蛋白作为致敏原建立大鼠哮喘模型,分离出大鼠的气道平滑肌细胞,用SNP(NO的供体)干预,通过四甲基偶氮唑蓝(MTT)法测定细胞生长率的变化,用原位末端标记法和流式细胞术检测SNP对哮喘大鼠气道平滑肌细胞细胞凋亡的影响。结果⑴MTT法测定:SNP+哮喘组的细胞抑制率明显高于哮喘组细胞存活率,(n=8,P<0.05),且呈浓度依赖关系。⑵TUNEL(原位末端标记)法检测:SNP+哮喘组的凋亡指数明显高于哮喘组,(n=4,P<0.05)。⑶流式细胞术测定SNP+哮喘组的平滑肌细胞凋亡率明显高于哮喘组,(n=4,P<0.05)。结论硝普钠能抑制哮喘大鼠气道平滑肌细胞的增殖,并且能诱导哮喘大鼠气道平滑肌细胞的凋亡,这种作用可能与治疗哮喘的气道重建有关。
Objective To explore the effects of Sodium Nitroprasside （SNP） on apoptosis of airway smooth muscle cells （ASMCs） of asthmatic rats in vitro. Methods Ten Wister rats were selected to make the models of asthma. The effect of SNP on the survival rate of asthmatic rat airway smooth muscle cells was detected by MTT method. The apoptosis of cells was detected by TUNEL method and flow cytometry. Results Comparing with asthma group, the survival rate of ASMCs was decreased significantly in SNP plus asthma group by MTT method （P 〈 0.05）. The apoptosis index of ASMCs was significantly increased following SNP treatment （P 〈 0.05）. Flow cytometry showed that the apoptosis rate of ASMCs was significantly increased following SNP treatment （P 〈 0.05）. Conclusion The treatment of SNP can inhibit the proliferation and induce apoptosis of asthmatic rat airway smooth muscle cells, which may be involved in treatment of airway remodeling in asthma.
出处
《中国医师杂志》
CAS
2006年第3期334-337,共4页
Journal of Chinese Physician
基金
国家自然科学基金资助项目(30270583)
