SMND-309对缺氧缺糖诱导的SH-SY5Y神经细胞凋亡的影响  

Neuroprotective Effects of SMND-309 on Apoptosis Induced by Oxygen-Glucose Deprivation in SH-SY5Y Cells

作　　者：姚晨[1] 杨建雄[1] 

机构地区：[1]陕西师范大学生命科学学院,西安710062

出　　处：《鲁东大学学报（自然科学版）》2011年第2期150-153,163,共5页Journal of Ludong University:Natural Science Edition

基　　金：国家科技部"重大新药创制"科技重大专项(2009ZX09103-006);国家自然科学基金(81001661)

摘　　要：体外培养人神经母细胞瘤细胞SH-SY5Y,利用缺氧、缺糖诱导细胞凋亡,采用SRB法测定细胞活力,比色法测定乳酸脱氢酶(LDH)活性,Hoechst33258荧光染色观察细胞凋亡,Western blotting测定凋亡相关蛋白Bcl-2和Bax含量.结果显示SMND-309能显著抑制SH-SY5Y细胞的凋亡,降低细胞损伤程度并提高细胞活力(p<0.05或p<0.01),这与其上调胞内抗凋亡蛋白Bcl-2表达密切相关,但对促凋亡蛋白Bax的表达影响不明显.The human neuroblastoma SH-SY5Y were cultured in a hypoxia/hypoglyc-emia condition to induce cell apoptosis in vitro.The viability of SH-SY5Y cells and level of lactate dehydrogenase（LDH） was measured by sulfonyl-rhodamine B（SRB） assay and colorimetric,respectively.The characteristic of apoptosis in morphological was observed with Hoechst33258 fluorescence staining,and Western blotting was used to detect the expression of Bcl-2 and Bax.The results in present study suggested that SMND-309 significantly restrained apoptosis of SH-SY5Y cells,degraded the degree of injury and elevated the cellular viability.These effects were correlated to the upregulation of Bcl-2,but not attributed to the change of Bax.

关 键 词：SMND-309 SH-SY5Y细胞 细胞凋亡 

分 类 号：R965.2[医药卫生—药理学] Q255[医药卫生—药学]