CAJ | 학술논문

目的：通过该研究探讨血管紧张素Ⅱ（AngⅡ）预处理对缺血缺氧条件下BM SCs的Bcl-2和Ba x的表达的影响，从而寻求减少BM SCs在缺血缺氧环境中凋亡的更好机制。方法以缺氧无血清（Ischemia）条件模拟心肌梗死后的缺血缺氧微环境。分离培养 SD 大鼠的BM SCs，传代后取生长状态良好的BM SCs进行缺血缺氧处理，细胞活力采用CCK-8试剂盒测定，以不同浓度的血管紧张素Ⅱ预处理BM SCs，缺血缺氧条件下培养24 h，提取BM SCs的总RNA进行RT-PCR检测Bcl-2及Bax的表达情况；Western blot法检测各组细胞Bcl-2及Bax的蛋白表达情况。结果与对照组相比，缺血缺氧组BM SCs 的细胞活力明显下降（P＜0.05）；与单纯缺血缺氧组比较，血管紧张素Ⅱ预处理组BM SCs的Bcl-2的表达上调（P＜0.05），Ba x的表达下调（P＜0.05），Bcl-2/Ba x比值增大（P＜0.05）。结论以缺氧无血清条件模拟细胞缺血缺氧条件下BM SCs 的增殖和细胞活力明显下降；血管紧张素Ⅱ可增强缺血缺氧条件下 BM SCs 的抗凋亡能力，这一过程可能是通过升高Bcl-2/Ba x比值来实现的。
목적：통과해연구탐토혈관긴장소Ⅱ（AngⅡ）예처리대결혈결양조건하BM SCs적Bcl-2화Ba x적표체적영향，종이심구감소BM SCs재결혈결양배경중조망적경호궤제。방법이결양무혈청（Ischemia）조건모의심기경사후적결혈결양미배경。분리배양 SD 대서적BM SCs，전대후취생장상태량호적BM SCs진행결혈결양처리，세포활력채용CCK-8시제합측정，이불동농도적혈관긴장소Ⅱ예처리BM SCs，결혈결양조건하배양24 h，제취BM SCs적총RNA진행RT-PCR검측Bcl-2급Bax적표체정황；Western blot법검측각조세포Bcl-2급Bax적단백표체정황。결과여대조조상비，결혈결양조BM SCs 적세포활력명현하강（P＜0.05）；여단순결혈결양조비교，혈관긴장소Ⅱ예처리조BM SCs적Bcl-2적표체상조（P＜0.05），Ba x적표체하조（P＜0.05），Bcl-2/Ba x비치증대（P＜0.05）。결론이결양무혈청조건모의세포결혈결양조건하BM SCs 적증식화세포활력명현하강；혈관긴장소Ⅱ가증강결혈결양조건하 BM SCs 적항조망능력，저일과정가능시통과승고Bcl-2/Ba x비치래실현적。
Objective To investigate angiotensinⅡ pretreatment in improving the Bcl-2 expression and reducing the expression of Bax in BMSCs under blood anoxic conditions and reducing the BMSCs apoptosis in ischemia anoxic conditions. Methods The BMSCs in SD rat were extract for primer culture and passage, the well growing cell were took to the ischemia hypoxia microenvironment after myocardial infarction, which were simulated by hypoxia serum-free conditions. The cell vitality were determinate by CCK-8 kits, then the cells were stimulated by different concentrations of angiotensinⅡfor 24 hours, the total RNA of BMSCs were extracted for detection the expression of Bcl-2 and Bax by RT-PCR. The total protein of BMSCs were extracted for detection the expression of Bcl-2 and Bax by Western blot. Results Compared with control group, the cell vitality of was obviously decreased (P<0.05). Compared with ischemia hypoxia group, the Bcl-2 expression increased and the Bax expression decreased in BMSCs in ischemia hypoxia group after stimulated by angiotensinⅡBMSCs (P<0.05), the Bcl-2/Bax ratio were increased (P<0.05). Conclusion BMSCs proliferation and cell activity decreased obviously in serum-free conditional simulation cell in hypoxia ischemia anoxic condition. AngiotensinⅡcan obviously increase antiapoptotic ability of BMSCs ischemia anoxic conditions. This process could be elevated by the Bcl-2/Bax ratio.