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    The aim of this study was to evaluate whether myosin light chain kinase (MLCK) knockdown attenuated H9C2 cell hypoxia/reoxygenation (H/R) injury and downstream signaling pathway. The MLCK expression in H/R injury model H9C2 cell was determined by western blot and qRT-PCR. H/R cells were transfected with si-MLCK in the presence of P38 inhibitor (SB203580) or ERK inhibitor (U0126). Then, cell apoptosis was verified by flow cytometry. Apoptosis-related proteins were detected by western blot. The contents of reactive oxygen species (ROS), lactate dehydrogenase (LDH), superoxide dismutase (SOD), interleukin-6 (IL-6), interleukin (IL)-1β (IL-1β), and tumor necrosis factor-α (TNF-α) were measured using flow cytometry and colorimetric assays, respectively. MLCK expression was higher in H/R cells. Knockdown of MLCK diminished the amounts of ROS, LDH, IL-6, IL-1β, and TNF-α and elevated the release of SOD in H/R model H9C2 cells. Additionally, H/R injury induced the cumulative expression and phosphorylation of ERK and the phosphorylation of P38, whereas MLCK siRNA-treated cells showed decreased ERK1/2 and P38 activation. Inversely, P38 inhibitor (SB203580) and ERK inhibitor (U0126) could reverse the cardioprotective effects induced by si-MLCK. MLCK knockdown attenuated H/R injury in H9C2 cells via regulating the ERK/P38 signaling pathway. MLCK/ERK/p38 axis may provide novel insight into therapeutic targets to restrain I/R injury caused by revascularization therapy after acute myocardial infarction. Copyright © 2022 Qibo Zhang et al.


    Qibo Zhang, Xiaoxiao Liu, Wen Yi, Chunquan Zhang. Myosin Light Chain Kinase Modulates to Improve Myocardial Hypoxia/Reoxygenation Injury. Journal of healthcare engineering. 2022;2022:8124343

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    PMID: 35378949

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