Al-Rasheed, Nawal M., Al-Rasheed, Nouf M., AL-Rabeeah, Danah A., AL-Barrak, Heba S., AL-Salman, Salma A., Ibrahim, Shahd A., AL-Hassab, Sulafa A., Al-Amin, Maha A., Hasan, Iman H., Al-Ajmi, Hanaa N., and AL-Shammari, Tahani K.
Journal of Cellular Biochemistry. May 2018, Vol. 119 Issue 5, p3903, 10 p.
Vitamin E -- Analysis and Hypoglycemic agents -- Analysis
Byline: Nawal M. Al-Rasheed, Nouf M. Al-Rasheed, Danah A. AL-Rabeeah, Heba S. AL-Barrak, Salma A. AL-Salman, Shahd A. Ibrahim, Sulafa A. AL-Hassab,Maha A. Al-Amin, Iman H. Hasan, Hanaa N. Al-Ajmi, Tahani K. AL-Shammari Abstract Several studies have reported that metformin is cardioprotective for diabetic and non-diabetic ischemic hearts through mechanisms that cannot be entirely attributed to its anti-hyperglycemic effect. This study was designed to investigate the cardioprotective effects of metformin with and without vitamin E after induction myocardial infarction (MI) in rats, using isoproterenol. Administration of metformin or vitamin E significantly reduced the cardiac mass index (P<0.01), ameliorated the changes to cardiac biomarkers, and attenuated oxidative stress levels compared to the isoproterenol group. Interestingly, combination therapy showed a slight synergistic effect. Histopathological analysis suggested that metformin treatment reduced NF-[PHI]B expression and protected against isoproterenol-induced MI. Our results indicate that metformin mediates a cardioprotective effect against isoproterenol-induced MI via antioxidant activity and modulation of the NF-[PHI]B signaling pathway. This suggests that metformin would be beneficial in MI treatment.