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

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 neuron...

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Bibliographic Details
Published inBiomolecules & therapeutics Vol. 27; no. 2; pp. 145 - 151
Main Authors Kang, Youra, Lee, Ji-Ha, Seo, Young Ho, Jang, Jung-Hee, Jeong, Chul-Ho, Lee, Sooyeun, Jeong, Gil-Saeng, Park, Byoungduck
Format Journal Article
LanguageKorean
Published 한국응용약물학회 01.03.2019
Subjects
Epicatechin
Methamphetamine
Neuroprotection
Neuroprotection
Methamphetamine
Epicatechin
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Summary: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.
Bibliography:The Korean Society of Applied Pharmacology
KISTI1.1003/JNL.JAKO201912964894783
ISSN:1976-9148
2005-4483