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首页> 外文期刊>Life sciences >Effect of advanced glycation end products on accelerated apoptosis of retinal capillary cells under in vitro conditions.
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Effect of advanced glycation end products on accelerated apoptosis of retinal capillary cells under in vitro conditions.

机译：高级糖基化终产物对体外条件下视网膜毛细血管细胞加速凋亡的影响。

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Advanced glycation end-products (AGEs) are considered to play an important role in the development of retinopathy in diabetes, and are shown to induce retinal vascular changes resembling that of diabetic retinopathy. We have shown that apoptosis of retinal capillary cells is accelerated in diabetes. The aim of this study is to investigate the role of AGEs in accelerated retinal capillary cell death in in vitro conditions, and to identify the possible mechanism involved. Bovine retinal endothelial cells and pericytes were incubated in the presence of 5 muM AGE-bovine serum albumin (AGE-BSA) or untreated control BSA (BSA) for up to five days. The cell death was determined by performing ELISA for cytoplasmic histone-associated DNA fragments and by measuring the activity of caspase-3. Incubation of endothelial cells or pericytes with AGE-BSA increased oxidative stress and NO by 60%, and in the same cells nuclear transcriptional factor (NF-kB) was also activated by over 60%. AGE-BSA induced their apoptosis by 55%, and activated caspase-3 by about 50% compared to the cells incubated with unmodified BSA. Co-addition of AGE-BSA and antioxidants (N-acetyl cysteine or alpha-lipoic acid) inhibited oxidative stress, nitrotyrosine formation, NF-kB activation and capillary cell apoptosis. These data strongly suggest that increased AGE in diabetes could play an important role in retinal capillary apoptosis and that oxidative stress is involved in this process. Inhibition of AGEs in the retinal capillary cells could prevent their apoptosis, and ultimately, the development of retinopathy in diabetes.
机译：晚期糖基化终产物（AGEs）被认为在糖尿病性视网膜病的发展中起着重要作用，并显示出可诱导类似于糖尿病性视网膜病的视网膜血管变化。我们已经证明在糖尿病中视网膜毛细血管细胞的凋亡被加速。这项研究的目的是调查在体外条件下AGEs在加速视网膜毛细血管细胞死亡中的作用，并确定可能的机制。牛视网膜内皮细胞和周细胞在5μMAGE-牛血清白蛋白（AGE-BSA）或未处理的对照BSA（BSA）存在下孵育最多五天。通过对胞质组蛋白相关的DNA片段进行ELISA并测量caspase-3的活性来确定细胞死亡。用AGE-BSA孵育内皮细胞或周细胞会使氧化应激和NO增加60％，在同一细胞中，核转录因子（NF-kB）也被激活超过60％。与未修饰的BSA孵育的细胞相比，AGE-BSA诱导了55％的细胞凋亡，激活了caspase-3约50％。 AGE-BSA和抗氧化剂（N-乙酰半胱氨酸或α-硫辛酸）的共同添加抑制氧化应激，硝基酪氨酸形成，NF-kB活化和毛细血管细胞凋亡。这些数据有力地表明，糖尿病中AGE的升高可能在视网膜毛细血管凋亡中起重要作用，并且氧化应激参与了这一过程。视网膜毛细血管细胞中AGEs的抑制可阻止其凋亡，并最终阻止糖尿病视网膜病变的发展。

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