Methanol extract of Desmodium gangeticum roots preserves mitochondrial respiratory enzymes, protecting rat heart against oxidative stress induced by reperfusion injury

  • Kurian G
  • Yagnesh N
  • Kishan R
  • et al.
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Abstract

Ischaemia and reperfusion result in mitochondrial dysfunction, with decreased oxidative capacity, loss of cytochrome c and generation of reactive oxygen species. The aim of this study was to evaluate the effect of a methanol extract of Desmodium gangeticum (L) DC (Fabaceae) (DG) on lipid per-oxidation and antioxidants in mitochondria and tissue homogenates of normal, ischaemic and ischaemia-reperfused rats. Myocardial lipid peroxidation products (thiobarbituric acid reactive substances; TBARS) in cardiac tissue homogenates and mitochondrial fractions were significantly increased during ischaemia reperfusion. Antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase (GPx) and glutathione reductase) in the myocardial tissue homogenate and mitochondria decreased significantly during ischaemia reperfusion, accompanied by a decreased activity of mitochondrial respiratory enzymes. Daily pretreatment of rats with DG (50 or 100 mgkg−1) orally for 30 days had a significant effect on the activity of mitochondrial and antioxidant enzymes. In-vitro studies showed that DG inhibited lipid peroxidation, and also scavenged hydroxyl and superoxide radicals. The concentrations required to scavenge 50% of the superoxide and hydroxyl radicals were 21 and 50.5 μgmL−1, respectively. Administration of DG to normal rats did not have any significant effect on any of the parameters studied. The results of our study showed that DG possesses the ability to scavenge the free radicals generated during ischaemia and ischaemia reperfusion and thereby preserves the mitochondrial respiratory enzymes that eventually lead to cardioprotection.

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Kurian, G. A., Yagnesh, N., Kishan, R. S., & Paddikkala, J. (2008). Methanol extract of Desmodium gangeticum roots preserves mitochondrial respiratory enzymes, protecting rat heart against oxidative stress induced by reperfusion injury. Journal of Pharmacy and Pharmacology, 60(4), 523–530. https://doi.org/10.1211/jpp.60.4.0016

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