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抑制可溶性环氧化酶可以预防糖尿病视网膜病变

Jiong Hu^1,2, Sarah Dziumbla^1,2, Jihong Lin³

¹Institute for Vascular Signalling, Centre for Molecular Medicine, Goethe University, Frankfurt am Main, Germany.

|December 7, 2017

概括

可溶性环氧化酶 (sEH) 通过损伤血管细胞和增加泄漏导致糖尿病视网膜病变. 在糖尿病小鼠中抑制sEH可以防止危及视力的血管损伤,这表明了新的治疗点.

科学领域:

眼科眼科
血管生物学
生物化学

背景情况:

糖尿病视网膜病变是导致成年人失明的主要原因.
其中包括血管细胞损失,屏障功能障碍,泄漏和新血管化.
驱动DR病变的潜在分子机制需要进一步阐明.

研究的目的:

确定涉及糖尿病视网膜病变的关键酶和分子通路.
研究可溶性环氧化酶 (sEH) 在DR病变发生过程中的作用.
评估SEH抑制对DR的治疗潜力.

主要方法:

在糖尿病小鼠和人类视网膜中评估了SEH表达和二醇水平.
使用基于细胞的测试来确定二醇诱导的血管损伤的机制.
给糖尿病小鼠使用特定的sEH抑制剂,并评估视网膜血管完整性.
在非糖尿病小鼠视网膜中过度表达sEH以评估其致病作用.

主要成果:

在糖尿病患者的视网膜中观察到sEH表达的增加和19. 20- 二氧化酸的积累.
由sEH衍生的二醇破坏了细胞膜蛋白质,破坏了细胞-细胞结合和细胞周内细胞相互作用.
在糖尿病小鼠中抑制sEH可以防止血管泄漏和细胞周损失.
在非糖尿病小鼠中,SEH过度表达模仿了DR类血管异常.

结论:

可溶性环氧化酶 (sEH) 是一种关键的酶,可在糖尿病视网膜病变中启动细胞周损失和内皮屏障功能障碍.
增加sEH表达是DR发病的一个关键驱动因素.
针对sEH是一种有前途的治疗策略,用于预防或治疗糖尿病视网膜病变.

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