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目的 研究糖基化终产物 (advancedglycosylationendproducts,AGE)对培养的牛视网膜毛细血管周细胞凋亡及凋亡调节基因Bax、bcl 2表达的影响 ,以探讨糖尿病视网膜病变的发病机制。方法 在体外培养 3～ 6代近融合的视网膜毛细血管周细胞中加入不同浓度的AGE(8、32、12 5、5 0 0及2 0 0 0mg/L)液 ,于 4d后检测不同浓度AGE对牛视网膜毛细血管周细胞凋亡及凋亡调节基因Bax、bcl 2表达的影响。结果 周细胞与AGE作用 4d后 ,呈现出典型的细胞凋亡特征 ;AGE促周细胞凋亡(r=0 878,P <0 0 1)和凋亡调节基因Bax的表达 (r=0 85 5 ,P <0 0 1)及抑制凋亡调节基因bcl 2的表达 (r=- 0 85 0 ,P <0 0 1)呈剂量依赖性 ;而周细胞凋亡率与Bax/bcl 2的比率呈正相关 (r=0 80 8,P<0 0 1)。结论 AGE能以剂量依赖的方式促进周细胞的凋亡 ,周细胞的凋亡率取决于凋亡调节基因Bax/bcl 2的比率。细胞凋亡是糖尿病视网膜病变中毛细血管周细胞早期丧失的一种方式。
Objective To investigate the effect of advanced glycosylation end products (AGE) on the apoptosis of cultured bovine retinal capillary pericytes and the expression of Bax and bcl 2 genes in order to explore the pathogenesis of diabetic retinopathy. Methods Different concentrations of AGE (8, 32, 125, 500 and 2000 mg / L) were added into the retinal capillary pericytes cultured in vitro for 3 to 6 generations. After 4 days, AGE On the apoptosis of retinal capillary pericytes and the expression of apoptosis regulatory genes Bax and bcl 2 in bovine retinal capillary. RESULTS: After treated with AGE for 4 days, the typical characteristics of apoptosis were showed. AGE promoted the expression of apoptosis-promoting gene Bax (r = 0 878, P 0 01) , P <0.01) and the expression of apoptosis-suppressing gene bcl 2 (r = - 0 85 0, P 0 01) in a dose-dependent manner. The ratio of apoptotic cells to Bax / bcl 2 was positive (R = 0 80 8, P <0 0 1). Conclusion AGE can promote apoptosis of pericytes in a dose-dependent manner. The rate of apoptosis of pericytes depends on the ratio of Bax / bcl 2. Apoptosis is a way of early loss of capillary pericytes in diabetic retinopathy.