Author/Authors :
Ghyasi, Rafigheh Applied Drug Research Center, Tabriz University of Medical Sciences, Tabriz, , Sepehri, Gholamreza Applied Drug Research Center, Tabriz University of Medical Sciences, Tabriz, , Mohammadi, Mustafa Applied Drug Research Center, Tabriz University of Medical Sciences, Tabriz, , Badalzadeh, Reza Applied Drug Research Center, Tabriz University of Medical Sciences, Tabriz, , Ghyasi, Akbar Applied Drug Research Center, Tabriz University of Medical Sciences, Tabriz,
Abstract :
Myocardial infarction (MI) is the acute condition of necrosis in myocardium which occurs as a result of imbalance
between coronary blood supply and myocardial demand. The resultant oxidative stress excess leads to worsen the condition. The
aim of this study was to investigate the effect of mebudipine, a new dihydropyridine calcium channel blocker, on lipid peroxidation
and antioxidant enzymes in myocardial ischemia‑reperfusion injury. Materials and Methods: Male Wistar rats (250‑300 g) were
randomly divided to Control‑ischemic, mebudipine‑ischemic and vehicle (ethanol‑ischemic) groups. The hearts of anaesthetized
rats were removed and mounted on Langendorff apparatus and perfused by Krebs‑Henseleit solution under constant pressure of
75 mmHg at 37°C. Ischemic groups were received 30 min global ischemia and 120 min reperfusion and the mebudipine and vehicle
groups received mebudipine (0.1 nM) or ethanol (0.01%)‑enriched solution 25 min before global ischemia. Malondialdehyde (MDA),
superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase levels of heart tissue samples were determined by
commercial specific Kits. Results: Mebudipine significantly reduced the MDA level (2.3 ± 0.07 nmol/mg protein) as the biochemical
indicator of oxidative damage and lipid peroxidation product as compared with those of vehicle (4.6 ± 0.01 nmol/mg protein) and
control groups (4.8 ± 0.09 nmol/mg protein). Furthermore, antioxidant enzymes SOD (0.1 ± 0.006 in drug vs. 0.037 ± 0.009 U/mg
Protein in control), GPX (16 ± 0.009 in drug vs. 0.068 ± 0.01 U/mg Protein in control) and catalase activities (0.075 ± 0.006 in
drug vs. 0.028 ± 0.002 U/mg Protein in control), activities of myocardium were significantly increased by mebudipine (P < 0.01).
Conclusion: Our results showed that mebudipine may have antioxidant activity against myocardial ischemia‑reperfusion injury
since it decreased oxidative stress by enhancing the enzymatic antioxidant defense and inhibiting the lipid peroxidation. Thus, this
drug can reduce the intensity of cardiac ischemic insults.
Keywords :
Ischemia , lipid peroxidation , mebudipine , myocardial , oxidative stress , reperfusion
