Epicatechin Prevents Methamphetamine-Induced Neuronal Cell Death via Inhibition of ER Stress
10.4062/biomolther.2018.092
- Author:
Youra KANG
1
;
Ji Ha LEE
;
Young Ho SEO
;
Jung Hee JANG
;
Chul Ho JEONG
;
Sooyeun LEE
;
Gil Saeng JEONG
;
Byoungduck PARK
Author Information
1. College of Pharmacy, Keimyung University, Daegu 42601, Republic of Korea. bdpark@kmu.ac.kr
- Publication Type:Original Article
- From:Biomolecules & Therapeutics
2019;27(2):145-151
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
