【摘要】：當(dāng)機(jī)體受到親電子物質(zhì)或活性氧刺激時(shí),核轉(zhuǎn)錄相關(guān)因子2(nuclear factor erythroid-2 related factor 2,Nrf2)能誘導(dǎo)出一系列的保護(hù)性蛋白,從而抵抗內(nèi)源性或外源性氧化應(yīng)激造成的損害。越來越多的研究發(fā)現(xiàn),某些組織比如心臟受到氧化應(yīng)激時(shí),Nrf2的活性和線粒體生物合成有關(guān)。在Surfeit 1蛋白(Surfeit locus protein 1,Surf1)突變的小鼠心臟中發(fā)現(xiàn),由于細(xì)胞色素C氧化酶的缺乏導(dǎo)致細(xì)胞呼吸減少從而激活Nrf2。本文從Kelch樣環(huán)氧氯丙烷相關(guān)蛋白1(Kelch-like ECH-associated protein-1,Keap1)-Nrf2通路與線粒體的關(guān)系以及氧化應(yīng)激條件下Nrf2信號(hào)通路與線粒體之間的信號(hào)交聯(lián)為重點(diǎn)進(jìn)行了綜述。
[Abstract]:When an organism is stimulated by an electron-friendly substance or reactive oxygen species (Ros), nuclear transcription-associated factor 2 (nuclear factor erythroid-2 related factor-2) can induce a series of protective proteins, thus resisting the damage caused by endogenous or exogenous oxidative stress. More and more studies have found that Nrf2 activity is associated with mitochondrial biosynthesis in certain tissues such as the heart under oxidative stress. In the heart of mice with Surfeit 1 protein (Surfeit locus protein 1, Surf1) mutation, it was found that the lack of cytochrome C oxidase (cytochrome C oxidase) results in the reduction of cellular respiration and activation of Nrf2.. The relationship between Kelch-like epichlorohydrin-associated protein 1 (Kelch-like ECH-associated protein-1,Keap1)-Nrf2 pathway and mitochondria and the signal cross-linking between Nrf2 signaling pathway and mitochondria under oxidative stress were reviewed in this paper.
【作者單位】： 三峽大學(xué)第一臨床醫(yī)學(xué)院、宜昌市中心人民醫(yī)院;三峽大學(xué)附屬仁和醫(yī)院;三峽大學(xué)醫(yī)學(xué)院中醫(yī)系國家中醫(yī)藥(腫瘤)管理局三級(jí)實(shí)驗(yàn)室;
【基金】：國家自然科學(xué)基金資助項(xiàng)目(編號(hào):81173612)
【分類號(hào)】：R3416
，

本文編號(hào)：2453932