Selenium attenuates sleep deprivation-induced myocardial injury by modulating inflammatory, circadian, and remodeling-related alterations

Sleep deprivation (SD) is an increasingly prevalent stressor that disrupts cardiovascular homeostasis. Given its antioxidant, anti-inflammatory, and cytoprotective properties, selenium may represent a promising candidate for limiting cardiovascular damage under physiological stress. This study investigated whether selenium supplementation attenuates SD-induced myocardial injury, with emphasis on oxidative stress and antioxidant defense, inflammatory signaling, extracellular matrix remodeling, and circadian clock regulation. Twenty-one male Wistar rats were assigned to control, SD, and SD+selenium (SD + Se) groups. Except for controls, animals were subjected to SD for 14 days. The SD + Se group was given sodium selenite (0.6 mg/kg/day, intraperitoneally). Cardiac MDA, SOD, IL-1β, IL-6, TGF-β, MMP-2, and MMP-9 levels were measured by ELISA. Histopathology was evaluated with hematoxylin-eosin staining, BMAL1, CLOCK, and CRY1 expression immunohistochemically, and NF-κB by immunofluorescence. In silico network and pathway enrichment analyses were conducted to identify molecular pathways linking selenium to circadian and stress-related signaling. SD markedly increased cardiac MDA, IL-1β, IL-6, TGF-β, NF-κB, MMP-2, and MMP-9 levels and, while decreasing SOD levels, was associated with severe myocyte degeneration, necrosis, and myocardial inflammation. It also altered the expression of BMAL1, CLOCK, and CRY1. Selenium supplementation significantly reduced IL-6, TGF-β, NF-κB, and MMP-2 levels, attenuated histopathological injury, and restored clock-related protein expression. In silico analysis identified six shared targets between sodium selenite-associated proteins and circadian regulators, enriched in oxidative stress, AP-1, TP53, cytokine, and MAPK pathways. These findings suggest that selenium supplementation may attenuate SD-induced myocardial injury through coordinated modulation of oxidative imbalance, inflammatory signaling, extracellular matrix remodeling, and circadian clock-related alterations. Thus, selenium may be a promising candidate for mitigating sleep deprivation-associated myocardial injury.