文章摘要

绿茶提取物表没食子儿茶素没食子酸酯对酒精诱导SH-SY5Y细胞损伤的作用研究

作者: 1杨海玉, 2刘勇, 3胡建新, 1文丽丹, 1巢海潮, 1曾红
1 江西省人民医院临床医学研究所,南昌 330006
2 江西省人民医院病理科,南昌 330006
3 江西省人民医院药剂科,南昌 330006
通讯: 刘勇 Email: jxpathology@126.com
DOI: 10.3978/j.issn.2095-6959.2016.12.002
基金: 江西省卫生厅中医药科研基金重点项目资助, 2013Z005

摘要

目的:体外观察绿茶提取物表没食子儿茶素没食子酸酯(epigallocatechin-3-gallate,EGCG)对酒精诱导SH-SY5Y细胞损伤的作用,初步探讨EGCG治疗酒精性痴呆(alcohol-associated dementia,AAD)的可行性。方法:以SH-SY5Y神经元细胞为实验对象,酒精组给予100 mol/L酒精37 ℃培养24 h,EGCG+酒精组在其培养液中同时加入不同浓度的EGCG(1~100 µmol/L)及100 mol/L酒精,37 ℃培养24 h;另设相同浓度的EGCG对照组(EGCG组)及空白对照组(对照组)。采用四甲基偶氮唑蓝(MTT)比色法检测细胞存活率,以Annexin-V APC/7-AAD双染法检测细胞凋亡及光镜下观察细胞形态。结果:MTT结果证实EGCG(25~100 µmol/L)作用24 h后可明显促进SH-SY5Y细胞存活,并呈浓度依赖关系(P<0.001)。流式检测及细胞形态观察结果证实酒精组细胞凋亡率(21.82%±1.27%),明显高于对照组(4.90%±0.80%)(P<0.001)及EGCG组(7.82%±0.68%)(P<0.001);EGCG(100 µmol/L)+酒精组细胞凋亡率(10.81%±0.31%),明显低于酒精组(P<0.001)。结论:EGCG可抑制酒精诱导SH-SY5Y细胞凋亡发生并促进细胞存活,提示EGCG对于AAD治疗具有潜在价值。
关键词: 表没食子儿茶素没食子酸酯 SH-SY5Y细胞 凋亡 酒精性痴呆

Effect of green tea compound epigallocatechin-3-gallate on alcohol-induced SH-SY5Y cell injury

Authors: 1YANG Haiyu, 2LIU Yong, 3HU Jianxin, 1WEN Lidan, 1CHAO Haichao, 1ZENG Hong
1 Institute of Clinical Medical Sciences, Jiangxi Provincial People’s Hospital, Nanchang 330006
2 Department of Pathology, Jiangxi Provincial People’s Hospital, Nanchang 330006
3 Department of Pharmacy, Jiangxi Provincial People’s Hospital, Nanchang 330006, China

CorrespondingAuthor: LIU Yong Email: jxpathology@126.com

DOI: 10.3978/j.issn.2095-6959.2016.12.002

Abstract

Objective: To observe in vitro effects of green tea compound epigallocatechin-3-gallate (EGCG) on alcohol-induced SH-SY5Y cell injury and discuss the feasibility of alcohol-associated dementia (AAD) treatment with EGCG. Methods: SH-SY5Y neuron cells were treated with ethanol (100 mol/L) for 24 h in 37 ℃ for ethanol group. In EGCG + ethanol group, cells were treated with different doses of EGCG (1—100 µmol/L) and ethanol (100 mol/L) for 24 h in 37 ℃. For control group or EGCG group, cells were treated only with cell medium or same doses of EGCG. The cell viability was analyzed with MTT assay. The staining with Annexin-V APC/7-AAD was used to observe cell apoptosis and the cell morphology was observed by optical microscope. Results: The cell survival was improved by treatment of EGCG for 24 h in a dose-dependent manner (25—100 µmol/L). Compared with control group (4.90%±0.80%) or EGCG group (7.82%±0.68%), cell apoptosis was apparently induced by treatment of ethanol (100 mol/L) for 24 h (21.82%±1.27%, P<0.001). However, co-treated with EGCG (100 µmol/L), these effects of ethanol on SH-SY5Y cells was prevented (10.81%±0.31%, P<0.001). Conclusion: EGCG inhibits alcohol-induced SH-SY5Y cell apoptosis and improve cell survival, which suggests that EGCG may have potential values for AAD treatment.

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