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ALDH2 保护自然衰老的小鼠视网膜，抑制氧化应激相关的细胞凋亡，并增强内质网中未折叠蛋白反应。

ALDH2 protects naturally aged mouse retina inhibiting oxidative stress-related apoptosis and enhancing unfolded protein response in endoplasmic reticulum.

机构信息

Department of General Practice, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, Shaanxi Province, China.

Department of Ophthalmology, The General Hospital of Western Theater Command, Chengdu 610083, Sichuan Province, China.

出版信息

Aging (Albany NY). 2020 Dec 19;13(2):2750-2767. doi: 10.18632/aging.202325.

DOI:10.18632/aging.202325
PMID:33411685
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7880320/
Abstract

During the process of aging, the retina exhibits chronic oxidative stress (OS) damage. Our preliminary experiment showed that acetaldehyde dehydrogenase 2 (ALDH2) could alleviate retinal damage caused by OS. This study aimed to explore whether ALDH2 could inhibit mice retinal cell apoptosis and enhance the function of unfolded protein response in endoplasmic reticulum (UPR) through reducing OS in aging process. Retinal function and structure and were examined in aged overexpression mice and ALDH2 agonist Alda1-treated aged mice. Levels of ALDH2, endoplasmic reticulum stress (ERS), apoptosis and inflammatory cytokines were evaluated. Higher expression of ALDH2 was observed at the outer nuclear layer (ONL) and the inner nuclear layer (INL) in aged overexpression and aged Alda1-treated mice. Moreover, aged overexpression mice and aged Alda1-treated mice exhibited better retinal function and structure. Increased expression of glucose-regulated protein 78 (GRP78) and ERS-related protein phosphorylated eukaryotic initiation factor 2 (peIF2α) and decreased expression of apoptosis-related protein, including C/EBP homologous protein (CHOP), caspase12 and caspase9, and retinal inflammatory cytokines were detected in the retina of aged overexpression mice and aged Alda1-treated mice. The expression of ALDH2 in the retina was decreased in aging process. ALDH2 could reduce retinal oxidative stress and apoptosis, strengthen UPR during the aging process to improve retinal function and structure.

摘要

在衰老过程中，视网膜会出现慢性氧化应激（OS）损伤。我们的初步实验表明，乙醛脱氢酶 2（ALDH2）可以减轻 OS 引起的视网膜损伤。本研究旨在探讨 ALDH2 是否可以通过减少衰老过程中的 OS 来抑制小鼠视网膜细胞凋亡并增强内质网（UPR）未折叠蛋白反应的功能。在过表达衰老小鼠和 ALDH2 激动剂 Alda1 处理的衰老小鼠中检查了视网膜功能和结构。评估了 ALDH2、内质网应激（ERS）、凋亡和炎症细胞因子的水平。在衰老的过表达和 Alda1 处理的小鼠的外核层（ONL）和内核层（INL）中观察到更高水平的 ALDH2 表达。此外，衰老的过表达小鼠和 Alda1 处理的衰老小鼠表现出更好的视网膜功能和结构。在衰老的过表达小鼠和 Alda1 处理的衰老小鼠的视网膜中，检测到葡萄糖调节蛋白 78（GRP78）和 ERS 相关蛋白磷酸化真核起始因子 2（peIF2α）的表达增加，以及凋亡相关蛋白，包括 C/EBP 同源蛋白（CHOP）、半胱天冬酶 12 和半胱天冬酶 9 的表达减少，以及视网膜炎症细胞因子的表达减少。ALDH2 在视网膜中的表达在衰老过程中减少。ALDH2 可以减轻视网膜氧化应激和凋亡，增强衰老过程中的 UPR，以改善视网膜功能和结构。

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