Bauhinia Championii Flavone Attenuates Hypoxia/reoxygenation Induced Apoptosis In H9c2 Cardiomyocytes Byactivating PI3L/Akt Pathway

Objective:This study aimed to determine the effects of Bauhinia championiiflavone(BCF)on hypoxia/reoxygenation(H/R)induced apoptosis in H9c2 cardiomyocytes and to explore potential mechanisms.Methods: The H/R model in H9c2 cardiomyocytes was established by 6 h of hypoxia and 12 h of reoxygenation.Cell viability was detected by CCK-8 assay.ATP production,LDH and MDA contentas well as CAT,SOD and GSH-Pxactivities were assessed by related assay kits.Apoptotic rate was measured by Annexin V/PI staining.Levels of mitochondria-associated ROS,mitochondrial membrane potential(??m)andmitochondrial permeability transition pore(MPTP)opening were assessed by fluorescent probes.The related proteinswere measured by western blotting.Results: Our results showed that pretreatment with BCF significantly improved cell viability,decreased LDH level,increased the antioxidant capacity and attenuated the cardiomyocyte apoptosis caused by H/R.Furthermore,BCF increased ATP production as well as inhibited ROS-generating mitochondria,depolarization of ??m,MPTP openingandcytochrome c release.Moreover,BCF pretreatment decreased Bax mitochondrial translocationas well as increased the ratio of Bcl-2 to Bax andthe expression of p-PI3 K and p-Akt.Interestingly,a specific inhibitor of phosphatidylinositol 3-kinase,LY294002,partly reversed the anti-apoptotic effect of BCF.Conclusions: These observations indicated that BCF pretreatment attenuates H/R-induced myocardial apoptosis strengthby improving mitochondrial dysfunctionvia PI3K/Akt signaling pathway.