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Sun, Mingchu, Zhang, Zihui, Yin, Yue, Yu, Lu, Jiang, Wenhua, Zhang, Chan, Gu, Chunhu, Ma, Heng, Wang, Yishi. (1402). Melatonin enhanced the cardioprotective effects of HTK solution on Langendorff-perfused mouse hearts subjected to ischemia/reperfusion. , 27(3), 366-374. doi: 10.22038/ijbms.2023.74152.16109
Mingchu Sun; Zihui Zhang; Yue Yin; Lu Yu; Wenhua Jiang; Chan Zhang; Chunhu Gu; Heng Ma; Yishi Wang. "Melatonin enhanced the cardioprotective effects of HTK solution on Langendorff-perfused mouse hearts subjected to ischemia/reperfusion". , 27, 3, 1402, 366-374. doi: 10.22038/ijbms.2023.74152.16109
Sun, Mingchu, Zhang, Zihui, Yin, Yue, Yu, Lu, Jiang, Wenhua, Zhang, Chan, Gu, Chunhu, Ma, Heng, Wang, Yishi. (1402). 'Melatonin enhanced the cardioprotective effects of HTK solution on Langendorff-perfused mouse hearts subjected to ischemia/reperfusion', , 27(3), pp. 366-374. doi: 10.22038/ijbms.2023.74152.16109
Sun, Mingchu, Zhang, Zihui, Yin, Yue, Yu, Lu, Jiang, Wenhua, Zhang, Chan, Gu, Chunhu, Ma, Heng, Wang, Yishi. Melatonin enhanced the cardioprotective effects of HTK solution on Langendorff-perfused mouse hearts subjected to ischemia/reperfusion. , 1402; 27(3): 366-374. doi: 10.22038/ijbms.2023.74152.16109

Melatonin enhanced the cardioprotective effects of HTK solution on Langendorff-perfused mouse hearts subjected to ischemia/reperfusion

Iranian Journal of Basic Medical Sciences
مقاله 14، دوره 27، شماره 3، خرداد 2024، صفحه 366-374    اصل مقاله (568.01 K)
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.22038/ijbms.2023.74152.16109
نویسندگان
Mingchu Sun* 1؛ Zihui Zhang1؛ Yue Yin2؛ Lu Yu3؛ Wenhua Jiang1؛ Chan Zhang1؛ Chunhu Gu4؛ Heng Ma2؛ Yishi Wang2
1Institute of Medical Research, Northwestern Polytechnical University, Xi’an Shaanxi, 710072 China
2Department of Physiology and Pathophysiology, School of Basic Medicine, Fourth Military Medical University, Xi’an, 710032 China
3Department of Pathology, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, China
4Department of Cardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, China
چکیده
Objective(s): Cardiac arrest is a crucial procedure in various cardiac surgeries, during which the heart is subjected to an ischemic state. The occurrence of ischemia/reperfusion (I/R) injury is inevitable due to aortic blockage and opening. The Histidine-tryptophan-ketoglutarate (HTK) solution is commonly used as an organ protection liquid to mitigate cardiac injury during cardiac surgery. Despite its widespread use, there is significant potential for improving its protective efficacy.
Materials and Methods: The cardioprotective effect of HTK solution with and without melatonin was evaluated using the isolated Langendorff-perfused mouse heart model. The isolated C57bL/6 mouse hearts were randomly divided into four groups: control, I/R, HTK solution treatment before reperfusion (HTK+I/R), and HTK solution combined with melatonin before reperfusion (HTK+M+I/R). Cardiac function and myocardial injury markers were then measured. AMP-activated protein kinase α2 (AMPKα2) KO mice were used to investigate the underlying mechanism.
Results: In our study, we found that melatonin significantly improved the protective effects of HTK solution in an isolated Langendorff-perfused mouse model, mechanistically by reducing mitochondrial damage, improving energy metabolism, inhibiting cardiomyocyte apoptosis, and reducing myocardial infarction size. We also observed that the HTK solution alone was ineffective in inhibiting ER stress, but when melatonin was added, there was a significant reduction in ER stress. Furthermore, melatonin was found to alleviate carbonyl stress during cardiac I/R. Interestingly, our results showed that the cardioprotective properties of melatonin were dependent on AMPKα2.
Conclusion: The findings presented in this study offer a valuable empirical foundation for the development of perioperative cardioprotective strategies.
کلیدواژه‌ها
Endoplasmic reticulum-stress؛ Heart protection؛ Langendorff heart؛ Melatonin؛ Myocardial ischemia/reperfusion injury
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