Zhang Li1, Zhenfeng Cheng1, Yu Haifeng1, Mengting Chen2, Lifang Li3. 1. Department of Cardiology, Huzhou Central Hospital, Huzhou, Zhejiang, China. 2. Department of Respiratory Medicine, Huzhou Central Hospital, Huzhou, Zhejiang, China. 3. Department of Cardiology, Huzhou Central Hospital, Huzhou, Zhejiang, China. Electronic address: fangll2017@163.com.
Abstract
BACKGROUND: Acute myocardial infarction (AMI) is a server disease effecting a large population worldwide. The pathophysiological process of ischemic/reperfusion (I/R) plays an important role for heart tissue damage. VO-OHpic, a PTEN inhibitor, has been demonstrated to be cardiac protective in sudden cardiac arrest models, but its role in AMI remains unclear. METHODS: An isolated AMI model was induced by dissecting the rat heart in a Langendorff system. Cardiac myocytes were extracted and induced ischemia in vitro. VO-OHpic was added into the above systems. The area of infarcted tissue in the heart was measured. Cardiac myocyte apoptosis was assessed by flow cytometry. Activation of Akt and GSK3β was quantified by flow cytometry. IL-10 levels were determined by ELISA. RESULTS: VO-OHpic reduced infarcted areas in the isolated heart, and improved cultured cardiac myocyte survival. VO-OHpic induced apoptosis resistance in cardiac myocytes. Akt-GSK3β signaling was activated by VO-OHpic administration. IL-10 levels in the medium were elevated by VO-OHpic. CONCLUSION: VO-OHpic protects heart tissue by apoptosis resistance via activating Akt-GSK3β signaling and increasing IL-10 levels.
BACKGROUND: Acute myocardial infarction (AMI) is a server disease effecting a large population worldwide. The pathophysiological process of ischemic/reperfusion (I/R) plays an important role for heart tissue damage. VO-OHpic, a PTEN inhibitor, has been demonstrated to be cardiac protective in sudden cardiac arrest models, but its role in AMI remains unclear. METHODS: An isolated AMI model was induced by dissecting the rat heart in a Langendorff system. Cardiac myocytes were extracted and induced ischemia in vitro. VO-OHpic was added into the above systems. The area of infarcted tissue in the heart was measured. Cardiac myocyte apoptosis was assessed by flow cytometry. Activation of Akt and GSK3β was quantified by flow cytometry. IL-10 levels were determined by ELISA. RESULTS:VO-OHpic reduced infarcted areas in the isolated heart, and improved cultured cardiac myocyte survival. VO-OHpic induced apoptosis resistance in cardiac myocytes. Akt-GSK3β signaling was activated by VO-OHpic administration. IL-10 levels in the medium were elevated by VO-OHpic. CONCLUSION:VO-OHpic protects heart tissue by apoptosis resistance via activating Akt-GSK3β signaling and increasing IL-10 levels.
Authors: Ana F Louro; Marta A Paiva; Marta R Oliveira; Katharina A Kasper; Paula M Alves; Patrícia Gomes-Alves; Margarida Serra Journal: Adv Sci (Weinh) Date: 2022-03-24 Impact factor: 17.521