| Summary: | <i>Background</i>: Radiation-induced heart injury can lead to increased risk of heart failure, attack, and ischemia. Some studies proposed IL-4 and IL-13 as two important cytokines that are involved in late effects of ionizing radiation. On the other hand, these cytokines may, through upregulation of <i>Duox1</i> and <i>Duox2</i>, induce chronic oxidative stress, inflammation, and fibrosis. In this study, we evaluated the upregulation of <i>Duox1</i> and <i>Duox2</i> pathways in hearts following chest irradiation in rats and then detected possible attenuation of them by melatonin. <i>Materials and Methods</i>: Twenty male Wistar rats were divided into four groups: (1) control; (2) melatonin treated (100 mg/kg); (3) radiation (15 Gy gamma rays); (4) melatonin treated before irradiation. All rats were sacrificed after 10 weeks and their heart tissues collected for real-time PCR (RT-PCR), ELISA detection of IL-4 and IL-13, as well as histopathological evaluation of macrophages and lymphocytes infiltration. <i>Results</i>: Results showed an upregulation of IL-4, <i>IL4ra1</i>, <i>Duox1</i>, and <i>Duox2</i>. The biggest changes were for <i>IL4ra1</i> and <i>Duox1</i>. Treatment with melatonin before irradiation could attenuate the upregulation of all genes. Melatonin also caused a reduction in IL-4 as well as reverse infiltration of inflammatory cells. <i>Conclusion</i>: <i>Duox1</i> and <i>Duox2</i> may be involved in the late effects of radiation-induced heart injury. Also, via attenuation of these genes, melatonin can offer protection against the toxic effects of radiation on the heart.
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