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绿茶多酚通过ROS-NO途径对SH-SY5Y细胞抵抗6-羟基多巴胺诱导的凋亡的保护作用。

Protective effect of green tea polyphenols on the SH-SY5Y cells against 6-OHDA induced apoptosis through ROS-NO pathway.

作者信息

Guo Shuhong, Bezard Erwan, Zhao Baolu

机构信息

Laboratory of Visual Information processing, Center of Brain & Cognitive Science, Institute of Biophysics, Academia Sinica, Beijing 100101, People's Republic of China.

出版信息

Free Radic Biol Med. 2005 Sep 1;39(5):682-95. doi: 10.1016/j.freeradbiomed.2005.04.022.

Abstract

Green tea polyphenols (GTP) are thought to help prevent oxidative stress-related diseases, such as cancer, cardiovascular disease, neurodegenerative disease, and aging. We here investigate the protective mechanisms of GTP on SH-SY5Y cells against apoptosis induced by the pro-parkinsonian neurotoxin 6-hydroxydopamine (6-OHDA). GTP rescued the changes in condensed nuclear and apoptotic bodies, attenuated 6-OHDA-induced early apoptosis, prevented the decrease in mitochondrial membrane potential, and suppressed accumulation of reactive oxygen species (ROS) and of intracellular free Ca(2+). GTP also counteracted the 6-OHDA-induced nitric oxide increase and overexpression of nNOS and iNOS, and decreased the level of protein-bound 3-nitrotyrosine (3-NT). In addition, GTP inhibited the autooxidation of 6-OHDA and scavenged oxygen free radicals in a dose- and time-dependent manner. Our results show that the protective effects of GTP on SH-SY5Y cells are mediated, at least in part, by controlling the ROS-NO pathway.

摘要

绿茶多酚(GTP)被认为有助于预防与氧化应激相关的疾病,如癌症、心血管疾病、神经退行性疾病和衰老。我们在此研究GTP对SH-SY5Y细胞的保护机制,以对抗帕金森病前体神经毒素6-羟基多巴胺(6-OHDA)诱导的细胞凋亡。GTP挽救了细胞核浓缩和凋亡小体的变化,减轻了6-OHDA诱导的早期凋亡,防止线粒体膜电位降低,并抑制活性氧(ROS)和细胞内游离Ca(2+)的积累。GTP还抵消了6-OHDA诱导的一氧化氮增加以及nNOS和iNOS的过表达,并降低了蛋白质结合的3-硝基酪氨酸(3-NT)水平。此外,GTP以剂量和时间依赖性方式抑制6-OHDA的自氧化并清除氧自由基。我们的结果表明,GTP对SH-SY5Y细胞的保护作用至少部分是通过控制ROS-NO途径介导的。

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