甲福明可以通过AMPK介导的线粒体融合来保护视网膜缺血/再输损伤
Kun Zhang1, Tao Wang2, Gui-Feng Sun3
1Institute of Geriatrics, Jiangxi Provincial People's Hospital & the First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi, 330006, PR China; Research Institute of Ophthalmology and Visual Sciences, Affiliated Eye Hospital of Nanchang University, Nanchang, Jiangxi, 330006, PR China; Department of Ophthalmology, Shenzhen People's Hospital & the Second Clinical Medical College of Jinan University, Shenzhen, Guangdong, 518020, PR China.
甲福明通过促进线粒体融合和减少有害的活性氧物种 (ROS) 来保护视网膜免受缺血/再损伤. 这种机制涉及AMPK的激活,这表明甲福林.
科学领域:
- 眼科医生 眼科 眼科
- 细胞生物学 细胞生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 视网膜缺血/反 (I/R) 损伤有助于视力丧失在条件,如青光眼和糖尿病视网膜病变.
- 甲胺是一种常见的糖尿病药物,在各种疾病模型中显示出潜力.
研究的目的:
- 调查甲福明对视网膜I/R损伤的保护作用.
- 阐明甲胺作用的潜在分子机制.
主要方法:
- 在R28细胞中诱导视网膜I/R损伤体内和模拟I/R (SIR).
- 评估视网膜厚度,细胞活力,线粒体功能 (Mfn2,OPA1,MMP,裂变) 和ROS水平.
- 使用AMPK抑制剂 (化合物C,siRNA) 和Mfn2/OPA1敲击.
主要成果:
- 甲胺缓解了I / R诱导的视网膜损伤和细胞损失.
- 甲胺通过上调Mfn2和OPA1.1,扭转了I/R诱导的线粒体功能障碍和裂变.
- AMPK激活对于甲胺对线粒体融合和ROS减少的影响至关重要.
结论:
- 甲胺通过AMPK介导的线粒体融合和降低线粒体ROS生成,保护视网膜I/R损伤.
- 甲胺作为治疗视网膜I / R损伤的治疗剂具有前途.
更多相关视频
07:14A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
Published on: July 13, 2018
08:43Simultaneous Measurement of Mitochondrial Calcium and Mitochondrial Membrane Potential in Live Cells by Fluorescent Microscopy
Published on: January 24, 2017
相关概念视频
Oral Hypoglycemic Agents: Biguanides and Glitazones
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
PI3K/mTOR/AKT Signaling Pathway
Dipeptidyl Peptidase 4 Inhibitors
