糖尿病性勃起功能障碍阴茎海绵体线粒体氧化应激损伤与保护机制研究
基本信息
结项摘要
糖尿病性勃起功能障碍（ED）发病机制十分复杂，涉及多个因素。我们前期研究发现糖尿病性ED大鼠阴茎海绵体内糖基化终产物（AGEs）沉积，氧自由基（ROS）堆积。而线粒体是机体内能量代谢和氧化中心，糖尿病状态下，线粒体氧化应激损伤使ROS进一步升高，加重氧化应激损伤，导致糖尿病的多种并发症发生发展。L-精氨酸、还原型谷胱甘肽均是ROS清除剂，通过提高线粒体ROS清除酶活性，来加速ROS的清除。L-精氨酸更可以作为NO通路的底物，促进NO产生。我们拟通过研究糖尿病性ED大鼠阴茎海绵体组织内线粒体结构与功能、酶活性和呼吸链等方面来观察其氧化应激损伤以及与凋亡的关系，并使用ROS清除剂来治疗糖尿病性ED，从勃起功能、自由基和线粒体功能、抗凋亡、NO通路、AGEs、NF-κB等多个作用途径来探索其治疗机制。线粒体氧化应激损伤是糖尿病性ED发病机制的一个重要补充，ROS清除剂更是治疗糖尿病性ED的新方法
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数据更新时间：2023-05-31
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