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一种与 AD 相关的神经保护剂可挽救 CoCl₂诱导的转化大鼠视网膜神经节细胞凋亡。

An AD-related neuroprotector rescues transformed rat retinal ganglion cells from CoCl₂-induced apoptosis.

机构信息

Department of Ophthalmology, Shengjing Hospital, China Medical University, Sanhao street 36, Heping district, Shenyang 110004, Liaoning Province, China.

出版信息

J Mol Neurosci. 2012 May;47(1):144-9. doi: 10.1007/s12031-011-9701-5. Epub 2012 Jan 5.

Abstract

Some ocular diseases characterized by apoptotic death of retinal ganglion cells (RGCs) and Alzheimer's disease (AD) are chronic neurodegenerative disorders and have similarities in neuropathology. Humanin (HN) is known for its ability to suppress neuronal death induced by AD-related insults. In present study, we investigated the neuroprotective effects of HN on hypoxia-induced toxicity in RGC-5 cells. Hypoxia mimetic compound cobalt chloride (CoCl₂) could increase the cell viability loss and apoptosis, whereas HN can significantly attenuate these effects. This finding may provide new therapeutics for the retinal neurodegenerative diseases targeting neuroprotection.

摘要

一些以视网膜神经节细胞(RGCs)凋亡死亡为特征的眼部疾病和阿尔茨海默病(AD)是慢性神经退行性疾病,其神经病理学具有相似性。人源素(HN)以其抑制 AD 相关损伤诱导的神经元死亡的能力而闻名。在本研究中,我们研究了 HN 对 RGC-5 细胞缺氧诱导毒性的神经保护作用。缺氧模拟化合物氯化钴(CoCl₂)可增加细胞活力损失和细胞凋亡,而 HN 可显著减轻这些作用。这一发现可能为针对神经保护的视网膜神经退行性疾病提供新的治疗方法。

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