Vitamin D Attenuates Myocardial Injury by Reduces ERK Phosphorylation Induced by I/R in Mice Model
Noor Ghaffar Said AL Habooby1, Nasser Ghaly Yousif2, *, Najah R. Hadi1, Jinan Jasim Al-Baghdadi2
Myocardial injury caused by ischemia followed by reperfusion mediates a complex series of inflammatory response that reduces the benefit of medical interventions, such as percutaneous coronary intervention, thrombolytic therapy, and coronary bypass surgery. Therefore, suppression of ischemia/reperfusion (I/R) -mediated myocardial injury is a high priority in clinical practice. The objective of this study was to investigate whether vitamin has some protective effect on heart after myocardial I/R, and the mechanistic pathway of this effect.
Adult (4 - 6 months) male Albino-Webster mice were randomly divided into 2 groups: (1) sham-control group, (2) ischemia and reperfusion (I/R) operated group, (3) vehicle-treated group, and (4) vitamin D-treated group receiving vitamin D 20 mg/kg once daily shortly before I/R. 72h later, hemodynamics and Evan blue staining were applied to evaluate cardiac function and area at risk (AAR). ELISA technique is applied to investigate myocardial and plasma expression of cytokines (IL-1β, IL-6, and TNF-α), chemokine (MCP-1), and cTn-I. In addition, the activity of pERK1/2 was analyzed by Western blot. Further, the ischemia changes and myocytes injured were examined by Hematoxylin and Eosin (H&E) stain.
The results demonstrated that the treatment of vitamin D markedly improved left ventricular function (LVF) in mice, and reduced plasma level of cTn-I as marker of cardiac injury. Moreover, the effects of vitamin D was associated with attenuations in both chemokine and cytokines expression following I/R, accompanied by down-regulation of activation of ERK1/2 pathway.
Together, the present study results show that the treatment with vitamin D was able to improve LV function after I/R, which was associated with the reductions of inflammatory response and activity of pERK1/2 as mechanistic of its action.
Correspondence: Address correspondence to this author at the Al Muthanna Medical School/ Al Muthanna University, Iraq; Tel: 009647825425669; E-mail: email@example.com