Alleviation of cardiac mitochondrial dysfunction and oxidative stress underlies the protective effect of vitamin D in chronic stress-induced cardiac dysfunction in rats.

Chronic stress is associated with oxidative stress and mitochondrial dysfunction. These mechanisms promote adverse cardiovascular events. Though many experimental studies have reported a protective effect of vitamin D (VitD) on cardiovascular system, its effect on cardiovascular system in case of chronic stress is not studied yet. The present study aimed to detect the effects of VitD treatment against chronic immobilization stress (CIS)-induced cardiac dysfunction, focusing mainly on mitochondrial function and oxidative stress in rats. CIS showed cardiac dysfunction as indicated by a significant decrease in the left ventricular end-diastolic and systolic diameters and decrease in ejection fraction and fractional shortening compared to the control group. This was accompanied by a significant decrease in tissue reserves of reduced glutathione (GSH), superoxide dismutase (SOD), ATP and cardiolipin as well as increase in malondialdehyde (MDA) and expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α). All these effects were accompanied by a significant increase in plasma adrenaline and noradrenaline. Treatment with VitD ameliorated all the aforementioned CIS-induced effects except PGC-1α expression in a dose-dependent manner. To our knowledge, this is the first study describing the prophylactic cardioprotective effects of VitD against CIS by targeting mitochondrial function.