Research article

Chronic garlic administration protects rat heart against oxidative stress induced by ischemic reperfusion injury

Sanjay Kumar Banerjee¹ , Amit Kumar Dinda² , Subhash Chandra Manchanda³ and Subir Kumar Maulik¹

¹  Department of Pharmacology, All India Institute of Medical sciences, New Delhi – 110029 India

²  Department of Pathology, All India Institute of Medical sciences, New Delhi – 110029 India

³  Department of Cardiology, All India Institute of Medical sciences, New Delhi – 110029 India

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BMC Pharmacology 2002, 2:16doi:10.1186/1471-2210-2-16

Published:	16 August 2002

Abstract

Background

Oxidative stress plays a major role in the biochemical and pathological changes associated with myocardial ischemic-reperfusion injury (IRI). The need to identify agents with a potential for preventing such damage has assumed great importance. Chronic oral administration of raw garlic has been previously reported to augment myocardial endogenous antioxidants. In the present study, the effect of chronic oral administration of raw garlic homogenate on oxidative stress induced by ischemic-reperfusion injury in isolated rat heart was investigated.

Results

Raw garlic homogenate (125, 250 and 500 mg/kg once daily for 30 days) was administered orally in Wistar albino rats. Thereafter, hearts were isolated and subjected to IRI (9 min. of global ischemia, followed by 12 min of reperfusion; perfusion with K-H buffer solution; 37°C, 60 mm Hg.). Significant myocyte injury and rise in myocardial TBARS along with reduction in myocardial SOD, catalase, GSH and GPx were observed following IRI. Depletion of myocardial endogenous antioxidants and rise in TBARS were significantly less in the garlic-treated rat hearts. Oxidative stress induced cellular damage as indicated by ultrastructural changes, like disruption of myofilament, Z-band architecture along with mitochondrial changes were significantly less.

Conclusions

The study strongly suggests that chronic garlic administration prevents oxidative stress and associated ultrastructural changes, induced by myocardial ischemic-reperfusion injury.