非吞噬细胞氧化酶1介导糖基化终末产物对牛视网膜周细胞凋亡的影响  

Non-phagocytic Cell Oxidase-1 Mediates Advanced Glycation End Products induced Apoptosis of Bovine Retinal Pericytes

作　　者：高凌[1] 李竞[1] 

机构地区：[1]武汉大学人民医院内分泌科,武汉430060

出　　处：《微循环学杂志》2013年第4期4-7,F0002,I0001,共6页Chinese Journal of Microcirculation

基　　金：国家自然科学基金资助项目(编号:81170767)

摘　　要：目的:探讨非吞噬细胞氧化酶1(NOX1)激活是否介导糖基化终末产物(AGE)对牛视网膜毛细血管周细胞(BRP)的凋亡。方法:将原代培养BRP分为3组:对照组、AGE组(200mg/L AGE)、干预组(200mg/L AGE+NOX1RNAi)。用锥蓝排斥法观察各组BRP的增殖,使用流式细胞术检测BRP凋亡水平,采用免疫杂交法检测活性Caspase-3的表达。结果:AGE组BRP增殖率较对照组明显降低;干预组则较AGE组明显升高(P均<0.01)。活性Caspase-3在AGE组表达上调,而在干预组表达降低(P均<0.01)。结论:AGE对BRP增殖的抑制或者促凋亡作用可能是通过激活Caspase-3实现,而信号通路NOX1的激活可能介导了AGE对Caspase-3的活化。Objective:To investigate whether non-phagocytic cell oxidase-1(NOX1)activation mediated the advanced glycation end products(AGE) induced apoptosis on bovine retinal pericytes(BRP).Method:Primary cultured BRP was divided into three groups:control group,AGE group(200mg/L)and intervention group(200mg/L AGE+NOX1 RNAi). Cone blue exclusion was used to examine the BRP proliferation and FACS was used to evaluate apoptosis;while immunoblotting assay was used to examine the protein expression of NOX1and activated caspase-3.Results: The proliferation was inhibited by AGE but reversed by NOX1silencing/intervention(both P<0.01).Moreover,NOX1silencing not only inhibited the AGE abetted caspase-3activation but also reversed AGE induced apoptosis(both P<0.01).Conclusion:AGE induced apoptosis or proliferation inhibition was possibly due to caspase-3activation,while NOX1activation in the signaling pathway may mediate AGE induced caspase-3activation.

关 键 词：晚期糖基化终末产物 周细胞凋亡 非吞噬细胞 牛视网膜 氧化酶1 糖尿病视网膜病变 视网膜毛细血管 慢性并发症 

分 类 号：R587.1[医药卫生—内分泌]