KMID : 0606920190270020145
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Biomolecules & Therapeutics 2019 Volume.27 No. 2 p.145 ~ p.151
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Epicatechin Prevents Methamphetamine-Induced Neuronal Cell Death via Inhibition of ER Stress
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Kang You-Ra
Lee Ji-Ha Seo Young-Ho Jang Jung-Hee Jeong Chul-Ho Lee Soo-Yeun Jeong Gil-Saeng Park Byoung-Duck
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Abstract
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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.
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KEYWORD
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Epicatechin, Methamphetamine, Neuroprotection
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