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J Physiol Biochem. 2013 Dec;69(4):937-44. doi: 10.1007/s13105-013-0272-5. Epub 2013 Jul 12.

Nigella sativa attenuates myocardial ischemic reperfusion injury in rats.

Author information

1
Physiology Department, Faculty of Medicine, Ain Shams University, 12 Abdullah Abu Elseoud Street, Triumph, Heliopolis, Cairo, Egypt, ansamseif@yahoo.com.

Abstract

Myocardial ischemia-reperfusion (I/R) represents a clinically relevant problem associated with thrombolysis, angioplasty, and coronary bypass surgery. Radical oxygen species generated during early reperfusion are the primary activator of mitochondrial permeability transition pore (MPTP) opening which finally results in cardiomyocyte death. Nigella sativa (NS) has been shown to have antioxidant properties. The present study aimed to determine whether supplementation with NS can provide sufficient protection for the myocardium against I/R insult and any possible role on mitochondrial MPTP. Adult male Wistar rats were allocated into two groups: control group and NS-treated group receiving NS (800 mg/kg) orally for 12 weeks. Rats' isolated hearts were perfused in Langendorff preparation to determine the baseline heart beating rate, developed peak tension, time to peak tension, rate of tension development, half relaxation time, and myocardial flow rate. Ischemia was then induced by stopping the perfusion fluid for 30 min, followed by 30 min of reperfusion and recording post I/R cardiac functions. Hearts were then used for assessment of malondialdehyde (MDA) and nicotinamide adenine dinucleotide (NAD(+)), since the hydrolysis of mitochondrial NAD(+) directly reflects MPTP opening in situ, and for histological examination. The NS-treated group showed enhanced post I/R contractile and vascular recovery, which was accompanied by elevated NAD(+) and decreased MDA compared to the control group. Histological examination showed marked improvement of cardiac musculature compared to the control group. In conclusion, N. sativa afforded substantial recovery of post I/R cardiac functions probably via inhibition of MPTP opening.

PMID:
23846789
DOI:
10.1007/s13105-013-0272-5
[Indexed for MEDLINE]

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