摘要
目的研究阻断p38途径对地塞米松(dexamethasone,DEX)诱导的胸腺细胞凋亡的影响。方法WesternBlott检测DEX对p38途径的阻断作用。以SB203580(SB)阻断BALB/c小鼠胸腺细胞p38途径,在3、5和7h,利用An-nexinV-FITC/PI双染流式细胞术检测细胞凋亡;利用DiOC6(3)/PI双染流式细胞术检测线粒体膜电势(△ψm)和细胞膜完整性变化。结果DEX显著减少了胸腺细胞p38蛋白含量;阻断p38后DEX诱导小鼠胸腺细胞晚期凋亡率显著增加(P<0.01);DEX诱导了胸腺细胞△ψm降低,同时阻断p38途径后,DiOC6(3)阴性PI阳性细胞显著增多(P<0.01)。结论阻断p38后加速了DEX介导的小鼠胸腺细胞凋亡中细胞膜完整性的破坏,该现象可能与线粒体功能有关。
Objective To study the effect of p38 inhibition on dexamethasone (DEX) induced thymocyte apoptosis. Methods The thymocytes were isolated from male Balb/c mice. p38 inhibition caused by DEX was detected with Western blotting, p38 pathway was blocked by SB203580 (SB), then the apoptosis was detected by Annexin V-FITC/PI double staining flow cytometry, the mitochondrial inner membrane potential ( △ψm ) and cell membrane integrity change were examined with DiOC6 (3)/PI double staining flow cytometry. Results DEX significantly reduced total p38 content in mouse thymocytes. The late phase rate of apoptosis induced by DEX was significantly increased by simultaneous p38 blocking. DEX induced thymocyte △ψm decrease and the DiOC6 (3) -PI^+ cells were significantly increased by simultaneous p38 blocking. Conclusion Cell membrane integrity loss in DEX induced mouse thymocyte apoptosis could be accelerated by p38 inhibition, and mitochon- drial function change may have relationship with it.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2006年第16期1667-1670,共4页
Journal of Third Military Medical University
基金
国家自然科学基金资助项目(30230350)
广东省自然科学基金资助项目(5300413)
暨南大学引进优秀人才科研启动基金资助项目(51204066)~~