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Open AccessArticle

Peroxiredoxin II Maintains the Mitochondrial Membrane Potential against Alcohol-Induced Apoptosis in HT22 Cells

1
College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing 163319, China
2
Library and Information Center, College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing 163319, China
3
School of Life Sciences, KNU Creative BioResearch Group (BK21 plus project), Kyungpook National University, Daegu 41566, Korea
4
Futuristic Animal Resource & Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju-si, Chungcheongbuk-do 28116, Korea
5
Primate Resources Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Jeongeup-si, Jeonbuk 56216, Korea
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Antioxidants 2020, 9(1), 1; https://doi.org/10.3390/antiox9010001
Received: 11 November 2019 / Revised: 17 December 2019 / Accepted: 17 December 2019 / Published: 18 December 2019
Excessive alcohol intake can significantly reduce cognitive function and cause irreversible learning and memory disorders. The brain is particularly vulnerable to alcohol-induced ROS damage; the hippocampus is one of the most sensitive areas of the brain for alcohol neurotoxicity. In the present study, we observed significant increasing of intracellular ROS accumulations in Peroxiredoxin II (Prx II) knockdown HT22 cells, which were induced by alcohol treatments. We also found that the level of ROS in mitochondrial was also increased, resulting in a decrease in the mitochondrial membrane potential. The phosphorylation of GSK3β (Ser9) and anti-apoptotic protein Bcl2 expression levels were significantly downregulated in Prx II knockdown HT22 cells, which suggests that Prx II knockdown HT22 cells were more susceptible to alcohol-induced apoptosis. Scavenging the alcohol-induced ROS with NAC significantly decreased the intracellular ROS levels, as well as the phosphorylation level of GSK3β in Prx II knockdown HT22 cells. Moreover, NAC treatment also dramatically restored the mitochondrial membrane potential and the cellular apoptosis in Prx II knockdown HT22 cells. Our findings suggest that Prx II plays a crucial role in alcohol-induced neuronal cell apoptosis by regulating the cellular ROS levels, especially through regulating the ROS-dependent mitochondrial membrane potential. Consequently, Prx II may be a therapeutic target molecule for alcohol-induced neuronal cell death, which is closely related to ROS-dependent mitochondria dysfunction. View Full-Text
Keywords: alcohol; ROS; oxidative damage; Prx II; neuronal cell alcohol; ROS; oxidative damage; Prx II; neuronal cell
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Jin, M.-H.; Yu, J.-B.; Sun, H.-N.; Jin, Y.-H.; Shen, G.-N.; Jin, C.-H.; Cui, Y.-D.; Lee, D.-S.; Kim, S.-U.; Kim, J.-S.; Kwon, T.; Han, Y.-H. Peroxiredoxin II Maintains the Mitochondrial Membrane Potential against Alcohol-Induced Apoptosis in HT22 Cells. Antioxidants 2020, 9, 1.

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