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作 者:谭家莉[1] 匡威[1] 段建民[1] 毕媛[2] 汪维建[1] 李潇[1] 段银钟[3] 刘彦普[4]
机构地区:[1]广州军区广州总医院口腔科,广东广州510000 [2]广州军区广州总医院医学实验科,广东广州510000 [3]第四军医大学口腔医学院正畸科,陕西西安710032 [4]第四军医大学口腔医学院口腔颌面外科,陕西西安710032
出 处:《临床口腔医学杂志》2011年第9期523-526,共4页Journal of Clinical Stomatology
基 金:国家自然科学基金资助(30900860);国家公派留学专项研究生奖学金项目(2009659007)
摘 要:目的:探讨高强度应力作用下体外培养成肌细胞凋亡的分子机制。方法:采用Flexercell Strain Unit系统对体外培养成肌细胞施加牵张应力,通过DNA ladder实验观察细胞凋亡情况。Western Blot检测磷酸化和总体JNK1的水平,通过NFkappa B报告系统检测其活性。通过JNK1的RNAi实验观察抑制JNK1后,是否补救被抑制的NFkappa B活性。结果:10%表面拉伸幅度的牵张应力作用24 h后,细胞形态梭形稍变长,且排列方向有一致性的趋势,DNA ladder实验证实15%以上较高强度应力引起C2C12细胞凋亡,高强度应力条件下成肌细胞凋亡过程中,JNK1通路被激活,抑制JNK1的活化,补救被抑制的NFkappa B活性。结论:高强度周期性牵张应力促进体外培养成肌细胞凋亡是通过激活JNK1通路而抑制NFkappa B活性实现的。Objective:To investigate the apoptosis mechanism of myoblasts C2C12 under cyclic stretch.Method:Flexercell Strain Unit was introduced to load cyclic stretch.DNA ladder experiment was used to test the apoptosis when they were loaded different stretches.Western blot was introduced to test pJNK1 level and NFkappaB reporter showed their activity.JNK1 RNAi was introduced to rescue NFkappaB.Result:When C2C12 cells were under 10 % cyclic stretch they began Spindle slightly longer.DNA ladder experiment showed when the stretch was more than 15 % it began to apoptosis.During this process pJNK1 increased while NFkappaB was inhibited.JNK1 RNAi could rescued NFkappaB inhibition.Conclusion:pJNK1 was increased when C2C12 myoblasts apoptosis under high stretch while NFkappaB was inhibited.
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