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Article

Transient Receptor Potential Melastatin 2 (TRPM2) Inhibition by Antioxidant, N-Acetyl-l-Cysteine, Reduces Global Cerebral Ischemia-Induced Neuronal Death

1
Department of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea
2
Department of Medical Science, College of Medicine, Hallym University, Chuncheon 24252, Korea
3
Division of Cardiovascular Diseases, Hallym University Medical Center, Anyang 14068, Korea
4
Department of Medical Education, College of Medicine, Hallym University, Chuncheon 24252, Korea
*
Authors to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(17), 6026; https://doi.org/10.3390/ijms21176026
Received: 9 July 2020 / Revised: 18 August 2020 / Accepted: 20 August 2020 / Published: 21 August 2020
(This article belongs to the Special Issue Neuroprotection: Rescue from Neuronal Death in the Brain)
A variety of pathogenic mechanisms, such as cytoplasmic calcium/zinc influx, reactive oxygen species production, and ionic imbalance, have been suggested to play a role in cerebral ischemia induced neurodegeneration. During the ischemic state that occurs after stroke or heart attack, it is observed that vesicular zinc can be released into the synaptic cleft, and then translocated into the cytoplasm via various cation channels. Transient receptor potential melastatin 2 (TRPM2) is highly distributed in the central nervous system and has high sensitivity to oxidative damage. Several previous studies have shown that TRPM2 channel activation contributes to neuroinflammation and neurodegeneration cascades. Therefore, we examined whether anti-oxidant treatment, such as with N-acetyl-l-cysteine (NAC), provides neuroprotection via regulation of TRPM2, following global cerebral ischemia (GCI). Experimental animals were then immediately injected with NAC (150 mg/kg/day) for 3 and 7 days, before sacrifice. We demonstrated that NAC administration reduced activation of GCI-induced neuronal death cascades, such as lipid peroxidation, microglia and astroglia activation, free zinc accumulation, and TRPM2 over-activation. Therefore, modulation of the TRPM2 channel can be a potential therapeutic target to prevent ischemia-induced neuronal death. View Full-Text
Keywords: global cerebral ischemia; N-acetyl-l-cysteine; transient receptor potential melastatin 2; zinc; neurodegeneration global cerebral ischemia; N-acetyl-l-cysteine; transient receptor potential melastatin 2; zinc; neurodegeneration
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MDPI and ACS Style

Hong, D.K.; Kho, A.R.; Lee, S.H.; Jeong, J.H.; Kang, B.S.; Kang, D.H.; Park, M.K.; Park, K.-H.; Lim, M.-S.; Choi, B.Y.; Suh, S.W. Transient Receptor Potential Melastatin 2 (TRPM2) Inhibition by Antioxidant, N-Acetyl-l-Cysteine, Reduces Global Cerebral Ischemia-Induced Neuronal Death. Int. J. Mol. Sci. 2020, 21, 6026. https://doi.org/10.3390/ijms21176026

AMA Style

Hong DK, Kho AR, Lee SH, Jeong JH, Kang BS, Kang DH, Park MK, Park K-H, Lim M-S, Choi BY, Suh SW. Transient Receptor Potential Melastatin 2 (TRPM2) Inhibition by Antioxidant, N-Acetyl-l-Cysteine, Reduces Global Cerebral Ischemia-Induced Neuronal Death. International Journal of Molecular Sciences. 2020; 21(17):6026. https://doi.org/10.3390/ijms21176026

Chicago/Turabian Style

Hong, Dae K., A R. Kho, Song H. Lee, Jeong H. Jeong, Beom S. Kang, Dong H. Kang, Min K. Park, Kyoung-Ha Park, Man-Sup Lim, Bo Y. Choi, and Sang W. Suh. 2020. "Transient Receptor Potential Melastatin 2 (TRPM2) Inhibition by Antioxidant, N-Acetyl-l-Cysteine, Reduces Global Cerebral Ischemia-Induced Neuronal Death" International Journal of Molecular Sciences 21, no. 17: 6026. https://doi.org/10.3390/ijms21176026

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