Dexmedetomidine Postconditioning Alleviates Hypoxia/Reoxygenation Injury in Senescent Myocardial Cells by Regulating lncRNA H19 and m⁶A Modification

Figure 8

Dex postconditioning protected aged H9c2 cells from aggravation of hypoxia/reperfusion (H/R) injury by ALKBH5 knockdown. H9c2 cells pretreated with H₂O₂ for 4 h were transfected with siALKBH5 or its NC 24 h later. Within 48 h of transfection, aged H9c2 cells were exposed to hypoxia for 6 h and either reoxygenation or Dex postconditioning for 6 h. (a) A CCK-8 assay was used to detect cell viability. (b) Flow cytometry was used to measure proportions of apoptotic cells. (c) Western blotting was used to evaluate protein expression of Bcl-2 and Bax. , , . (d) Schematic showing mechanisms of action for Dex in aged cardiomyocytes following H/R. ALKBH5 expression was decreased following H/R in senescence cardiomyocytes but thus was attenuated by Dex postconditioning. m⁶A methylation levels and H19 expression were regulated by ALKBH5. H19 expression was decreased following H/R. Subsequently, isolated miR-29b-3p increased binding to the 3-UTR region of cIAP1 and decreased its expression, leading to increased apoptosis.

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