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. 2021 Aug 13;8:654969. doi: 10.3389/fcvm.2021.654969

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Copyright © 2021 Du, Chen, Wu, Xia, Chen, Zhao, Wang, Yao, Liu, Zhang, Wang, Yang and Wang.

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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N1LR attenuated the cell death and LDH release of H9c2 cells. (A) Cell Death rates were measured to confirm the successful establishment of the hypoxia model. (B) The expression of N1LR was down-regulated with continuous exposure to hypoxia-induced by CoCl₂. (C) The expression of N1LR was down-regulated with continuous exposure to hypoxia-induced by H₂O₂. (D) The overexpression of N1LR was verified through qRT-PCR. (E) N1LR reduced the release of LDH in H₂O₂-treated H9c2 cells. (F) N1LR reduced the release of LDH in CoCl₂-treated H9c2 cells. (G) The H9c2 cell death was decreased in the N1LR+H₂O₂ group compared with the H₂O₂ group. (H) The H9c2 cell death was as well decreased in the N1LR+CoCl₂ group compared with the CoCl₂ group. **p < 0.01, ***p < 0.001 vs. NC group. ^#p < 0.05 vs. H₂O₂+NC or CoCl₂+NC group. Data were shown as means ± SD.