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| Protective effect of Irisin on damage of H9C2 cardiomyocytes under hypoxia-reoxygenation |
| WU Juan1 ZHANG Xiaomeng1 CHANG Pan1 ZHU Xiaoxing2 LI Jing1 WANG Xihui1 WANG Jianbang1 YU Jun3 |
1.Department of General Medicine, the Second Affiliated Hospital of Xi′an Medical College and Clinical Research Center of Cardiovascular Diseases, Shaanxi Province, Xi′an 710038, China;
2.Department of Ultrasound, Xijing Hospital, Air Force Military Medical University, Shaanxi Province, Xi′an 710036, China;
3.Clinical Experiment Center, Xi′an International Medical Center, Shaanxi Province, Xi′an 710100, China |
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Abstract Objective To observe the protective effect of Irisin on H9C2 cardiomyocytes after hypoxia reoxygenation. Methods Rat H9C2 cardiomyocytes were divided into control group, control+Irisin group, hypoxia-reoxygenation group, hypoxia-reoxygenation+Irisin group. The control group was cultured normally. The control +Irisin group was cultured normally and given 10 ng/mL of Irisin. The hypoxia-reoxygenation group was treated with hypoxia-reoxygenation, and the cells of hypoxia-reoxygenation+Irisin group were treated with hypoxia-reoxygenation and 10 ng/mL of Irisin. Cell viability was detected by CCK-8. Reactive exygen species (ROS) fluorescence probe was used to detect intracellular ROS, and mitochondrial membrane potential JC-1 was detected by flow cytometry. The mRNA levels of caspase-3 and caspase-9 in cardiomyocytes were detected by RT-PCR. Results The cell viability of the hypoxia-reoxygenation group was significantly lower than control group (P ＜ 0.01). The cell viability of the hypoxia-reoxygenation + Irisin group was higher than hypoxia-reoxygenation group (P ＜ 0.05). The intracellular ROS level in the hypoxia-reoxygenation group was higher than that in the control group (P ＜ 0.01). The level of ROS in the hypoxia-reoxygenation + Irisin group was lower than that of the hypoxia-reoxygenation group (P ＜ 0.05). The mitochondrial membrane potential JC-1 level in hypoxia-reoxygenation group was lower than control group (P ＜ 0.05). The level of mitochondrial membrane potential JC-1 in hypoxia-reoxygenation + Irisin group was higher than hypoxia-reoxygenation group (P ＜ 0.05). The mRNA levels of caspase-3 and caspase-9 in the hypoxia-reoxygenation group were higher than the control group (P ＜ 0.05). The mRNA levels of caspase-3 and caspase-9 in hypoxia-reoxygenation + Irisin group were lower than hypoxia-reoxygenation group (P ＜ 0.05). Conclusion Irisin can significantly improve the cell viability of cardiomyocytes after hypoxia-reoxygenation, reduce ROS production, restore mitochondrial membrane potential, and inhibit apoptosis pathway. It can be used as a potential therapeutic agent for improving myocardial ischemia-reperfusion injury.
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