Bauhinia championii Flavone Attenuates Hypoxia-Reoxygenation Induced Apoptosis in H9c2 Cardiomyocytes by Improving Mitochondrial Dysfunction

• Published in: Molecules (Basel, Switzerland) Vol. 21; no. 11; p. 1469
• Main Authors: Liao, Ping, Sun, Guibo, Zhang, Chan, Wang, Min, Sun, Yao, Zhou, Yuehan, Sun, Xiaobo, Jian, Jie
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 04.11.2016; MDPI
• Subjects: Animals; Apoptosis; Apoptosis - drug effects; Bauhinia; Bauhinia - chemistry; Bauhinia championii flavone; Cardiomyocytes; Cardiovascular disease; Cell Hypoxia - drug effects; Cell Line; Cell Survival - drug effects; Cytochrome; Flavones - isolation & purification; Flavones - pharmacology; Hypoxia; hypoxia-reoxygenation; Ischemia; Kinases; Membrane Potential, Mitochondrial - drug effects; Mitochondria - drug effects; mitochondrial dysfunction; Mitochondrial Membrane Transport Proteins - drug effects; Myocytes, Cardiac - cytology; Myocytes, Cardiac - drug effects; Oxygen - metabolism; PI3K/Akt; Rats; Reactive Oxygen Species - metabolism; China; apoptosis; mitochondrial dysfunction; hypoxia-reoxygenation; Bauhinia championii flavone; PI3K/Akt
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules21111469

This study aimed to determine the effects of flavone (BCF) on hypoxia-reoxygenation (H/R) induced apoptosis in H9c2 cardiomyocytes and to explore potential mechanisms. 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. Apoptotic rate was measured by Annexin V/PI staining. Levels of mitochondria-associated ROS, mitochondrial transmembrane potential (∆Ψm) and mitochondrial permeability transition pores (MPTP) opening were assessed by fluorescent probes. ATP production was measured by ATP assay kit. The release of cytochrome c, translocation of Bax, and related proteins were measured by western blotting. Our results showed that pretreatment with BCF significantly improved cell viability and attenuated the cardiomyocyte apoptosis caused by H/R. Furthermore, BCF increased ATP production and inhibited ROS-generating mitochondria, depolarization of ΔΨm, and MPTP opening. Moreover, BCF pretreatment decreased Bax mitochondrial translocation, cytochrome c release, and activation of caspase-3, as well as increased the expression of p-PI3K, p-Akt, and the ratio of Bcl-2 to Bax. Interestingly, a specific inhibitor of phosphatidylinositol 3-kinase, LY294002, partly reversed the anti-apoptotic effect of BCF. These observations indicated that BCF pretreatment attenuates H/R-induced myocardial apoptosis strength by improving mitochondrial dysfunction via PI3K/Akt signaling pathway.