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. 2020 Oct 23;8:598078. doi: 10.3389/fcell.2020.598078

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Copyright © 2020 Liu, Li and Huang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mitofusin 2 (Mfn2) overexpression attenuates mitochondrial ischemia–reperfusion (mI/R)-mediated neural death through inhibition of apoptosis. (A) Hypoxia–reoxygenation was used to mimic I/R (mI/R) injury in vitro. Then, RNA was isolated to analyze the transcription of Mfn2 in N2a cells. (B) Proteins were isolated from mI/R-treated N2a cells, and the expression of Mfn2 was determined through Western blots. (C) Cell viability was measured through cell counting kit-8 (CCK8) assay. (D) A lactate dehydrogenase (LDH) release assay was used to evaluate cell death. (E) ELISA for caspase-3 activity. (F,G) Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was used to evaluate cell apoptosis. ^∗P < 0.05.