Dexmedetomidine Ameliorates X-Ray-Induced Myocardial Injury Via Alleviating Cardiomyocyte Apoptosis and Autophagy

Abstract

Background Radiotherapy is one of the major local treatments for tumors. However, some complications may occur during the treatment, which includes radiation-induced heart disease (RIHD). However, there is no uniform standard for the prevention of RIHD currently. Dexmedetomidine is reported to have cardio protection effects, while its role in radiation-induced myocardial injury is unknown. In the current study, we aimed to evaluate the radioprotective effect of dexmedetomidine in X-ray radiation-treated mice. Methods 9 male mice were randomized into 3 groups: control, 16Gy, and 16Gy + Dex. The 16Gy group was exposed to a single dose of 16Gy X-ray radiation. 16Gy + Dex group was pretreated with dexmedetomidine before X-ray radiation. The control group was treated with saline and did not receive X-ray radiation. The myocardial tissues were collected 16 weeks after X-ray radiation and subjected to hematoxylin-eosin (HE) staining, TUNEL staining, and immunohistochemistry (IHC) staining. Besides, we established a radiation-injured cardiomyocyte model. Cell viability was assessed with CCK-8 assay and cell apoptosis was assessed using flow cytometry. Protein expression of Bcl-2, Bax, LC3 I/II, Beclin-1, and p62 was detected through western blot assay. Results The results showed that 16Gy X-ray radiation resulted in significant changes in myocardial tissues, increased myocardial apoptosis, and activated autophagy. Pretreatment with dexmedetomidine significantly protects mice against 16Gy X-ray radiation-induced myocardial injury by inhibiting apoptosis and autophagy. Conclusion In summary, our study confirmed the radioprotective effect of dexmedetomidine against 16Gy X-ray radiation-induced cardiomyocyte apoptosis and autophagy activation.