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. 2020 Apr 3;19(6):3581–3588. doi: 10.3892/etm.2020.8644

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Copyright: © Yu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Effect of the miR-663b inhibitor on H9c2 hypoxia-induced cell injury. (A) miR-663b expression in transfected H9c2 cells. (B) mRNA expression of BCL2L1 in transfected H9c2. (C) BCL2L1 mRNA and (D) protein levels in transfected H9c2 cells. Release of (E) CK-MB and (F) cTnI. (G) Mitochondrial viability. Data are presented as the mean ± standard deviation of three independent experiments. ^**P<0.01 vs. control group; ^##P<0.01 vs. hypoxia group; ^&&P<0.01 vs. hypoxia + inhibitor group. miR, microRNA; BCL2L1, B-cell lymphoma 2 like 1; siRNA, small interfering RNA; CK-MB, creatine kinase-muscle/brain; CTn1, Cardiac troponin 1.

Effect of the miR-663b inhibitor on H9c2 hypoxia-induced cell injury. (A) miR-663b expression in transfected H9c2 cells. (B) mRNA expression of BCL2L1 in transfected H9c2. (C) BCL2L1 mRNA and (D) protein levels in transfected H9c2 cells. Release of (E) CK-MB and (F) cTnI. (G) Mitochondrial viability. Data are presented as the mean ± standard deviation of three independent experiments. ^**P<0.01 vs. control group; ^##P<0.01 vs. hypoxia group; ^&&P<0.01 vs. hypoxia + inhibitor group. miR, microRNA; BCL2L1, B-cell lymphoma 2 like 1; siRNA, small interfering RNA; CK-MB, creatine kinase-muscle/brain; CTn1, Cardiac troponin 1.