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作 者:王子高[1] 王冠群[1] 杨雅松[1] 祖衡兵[1]
机构地区:[1]复旦大学附属金山医院神经内科,上海201508
出 处:《神经解剖学杂志》2015年第5期639-644,共6页Chinese Journal of Neuroanatomy
基 金:上海市金山区卫计委青年项目(JSKJ-KTQN-2014-08)
摘 要:目的:探讨胰岛素样生长因子-1(IGF-1)对β淀粉样蛋白25-35(beta-amyloid 25-35,Aβ25-35)诱导的神经母细胞瘤细胞(SH-SY5Y细胞)凋亡的影响。方法:以SH-SY5Y细胞系为研究对象,将其分为对照组、Aβ25-35组和IGF-1预处理组。利用Cell Counting Kit-8(CCK-8)试剂盒检测细胞活性;Annexin V-FITC/PI双染色法检测细胞凋亡率;Western blot检测Bcl-x L、Bax及cleaved caspase-3的表达。结果:Aβ25-35可降低SH-SY5Y细胞活性,诱导其发生细胞凋亡。IGF-1预处理组细胞活性增加,细胞凋亡率降低,伴有Bcl-x L表达增加、Bax表达降低及casapse-3活化减少。结论:IGF-1可通过上调Bcl-x L、下调Bax的表达,抑制casapse-3的活化,发挥抗Aβ25-35诱导的细胞凋亡作用。Objective: To explore the protective effect of insulin-like growth factor-1 (1GF-1) on Aβ25-35-induced apop- tosis in SH-SYSY cells, nethods:SH-SYSY cells were treated with different concentration of Aβ25-35 and IGF-1. Cell via- bility was detected by CCK-8. Apoptosis was measured by Annexin V-FITC/PI staining. Expression of Bcl-xL,Bax and cleaved caspase-3 was determined by Western blot. Results:Aβ25-35 inhibited cell viability and induced apoptosis in SH- SY5Y cells. Pretreatment with IGF-1 could significantly revesed the cytotoxicity effect of Aβ25-35, and IGF-1 could in- crease the ratio of Bcl-xL/Bax and inhibit the activation of caspase-3. Conclusion:These results indicate that IGF-I pro- tect SH-SY5Y cell from apoptosis induced by Aβ25-35 through increase of Bcl-xL/Bax and inactivation of caspase-3.
关 键 词:胰岛素样生长因子-1 AΒ25-35 凋亡 BCL-X L BAX caspase-3
分 类 号:R749.16[医药卫生—神经病学与精神病学]
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