Epicatechin Prevents Methamphetamine-Induced Neuronal Cell Death via Inhibition of ER Stress

被引：23

作者：

Kang, Youra ^{[1
]}

Lee, Ji-Ha ^{[1
]}

Seo, Young Ho ^{[1
]}

Jang, Jung-Hoe ^{[2
]}

Jeong, Chul-Ho ^{[1
]}

Lee, Sooyoun ^{[1
]}

Jeong, Gil-Saeng ^{[1
]}

Park, Byoungduck ^{[1
]}

机构：

[1] Keimyung Univ, Coll Pharm, Daegu 42601, South Korea

[2] Keimyung Univ, Sch Med, Dept Pharmacol, Daegu 42601, South Korea

来源：

BIOMOLECULES & THERAPEUTICS | 2019年 / 27卷 / 02期

基金：

新加坡国家研究基金会;

关键词：

Epicatechin; Methamphetamine; Neuroprotection; ENDOPLASMIC-RETICULUM STRESS; LIPID-PEROXIDATION; INDUCED APOPTOSIS; OXIDATIVE STRESS; CANCER-CELLS; ACTIVATION; RECEPTORS; TOXICITY; TRAIL; NEUROTOXICITY;

D O I：

10.4062/biomolther.2018.092

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Methamphetamine (METH) acts strongly on the nervous system and damages neurons and is known to cause neurodegenerative diseases such as Alzheimer's and Parkinson's. Flavonoids, polyphenolic compounds present in green tea, red wine and several fruits exhibit antioxidant properties that protect neurons from oxidative damage and promote neuronal survival. Especially, epicatechin (EC) is a powerful flavonoid with antibacterial, antiviral, antitumor and antimutagenic effects as well as antioxidant effects. We therefore investigated whether EC could prevent METH-induced neurotoxicity using HT22 hippocampal neuronal cells. EC reduced METH-induced cell death of HT22 cells. In addition, we observed that EC abrogated the activation of ERK, p38 and inhibited the expression of CHOP and DR4. EC also reduced METH-induced ROS accumulation and MMP. These results suggest that EC may protect HT22 hippocampal neurons against METH-induced cell death by reducing ER stress and mitochondrial damage.

引用

页码：145 / 151

页数：7

共 49 条

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