黑色素改善了Schwann细胞中高葡萄糖诱导的自
Hagar Mohamed Ahmed Salem1, Kian Chung Chok2, Rhun Yian Koh3
1School of Medicine, University of Liverpool Liverpool L69 3BX, England, United Kingdom.
概括
Melatonin 通过减少 Schwann 细胞中有害的自和内分泌网膜应激来保护糖尿病神经病变中的高葡萄糖诱导的神经损伤. 这种英多尔激素提供了显著的神经保护.
科学领域:
- 生物化学 生物化学
- 神经科学是一个神经科学.
- 细胞生物学 细胞生物学
背景情况:
- 糖尿病神经病变 (DN) 涉及高葡萄糖和自由基的神经损伤.
- 氨酸是一种内醇激素,通过自细胞调节显示出神经保护的潜力.
研究的目的:
- 在高葡萄糖条件下研究黑激素对施万细胞的神经保护作用.
- 阐明黑激素在调节DN中自和内细胞网膜 (ER) 应激中的作用.
主要方法:
- 使用MTT测定评估的细胞活力.
- 通过阿克里丁色染物观察到的自细胞激活.
- 蛋白质表达与自和ER压力相关,由西方杂志分析.
主要成果:
- 在1μM的黑表明最大的保护高葡萄糖诱导的细胞死亡.
- 黑色素 (5和10μM) 有效地降低了高葡萄糖诱导的自.
- 在 Schwann 细胞中,黑色素降低了自标志物 LC3 和 ER 压力标志物 (ATF4,ATF6,CHOP,PERK,eIF2-α) 的上调.
结论:
- 黑色素减轻高葡萄糖诱导的自在施万细胞.
- 这种保护机制涉及PERK-eIF2α-ATF4-CHOP信号通路.
- 黑素对糖尿病神经病变并发症具有显著的神经保护潜力.
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