Biomol Ther 2019; 27(2): 145-151
Epicatechin Prevents Methamphetamine-Induced Neuronal Cell Death via Inhibition of ER Stress
Youra Kang1, Ji-Ha Lee1, Young Ho Seo1, Jung-Hee Jang2, Chul-Ho Jeong1, Sooyeun Lee1, Gil-Saeng Jeong1,* and Byoungduck Park1,*
1College of Pharmacy, Keimyung University, Daegu 42601,
2Department of Pharmacology, School of Medicine, Keimyung University, Daegu 42601, Republic of Korea
E-mail: (Park B), (Jeong GS)
Tel: +82-53-580-6653 (Park B), +82-53-580-6649 (Jeong GS)
Fax: +82-53-580-6645 (Park B), +82-53-580-6645 (Jeong GS)
Received: May 21, 2018; Revised: June 11, 2018; Accepted: June 26, 2018; Published online: December 5, 2018.
© The Korean Society of Applied Pharmacology. All rights reserved.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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.
Keywords: Epicatechin, Methamphetamine, Neuroprotection

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Funding Information
  • National Research Foundation of Korea
      NRF-2016R1A6A1A03011325, NRF-2016R1A1A1A05921696

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