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Curcuminoids modulates oxidative damage and mitochondrial dysfunction in diabetic rat brain. | LitMetric

Curcuminoids modulates oxidative damage and mitochondrial dysfunction in diabetic rat brain.

Free Radic Res

Centre for Advanced Research in Indian System of Medicine, SASTRA University, Thanjavur, Tamilnadu, India.

Published: November 2008

AI Article Synopsis

  • Diabetes worsens brain injury by increasing oxidative damage and harming mitochondria due to high blood sugar levels.
  • The study examines how curcuminoids from Curcuma longa can help reduce oxidative stress and restore mitochondrial function in the brains of rats with diabetes induced by streptozotocin (STZ).
  • Results show that curcuminoid treatment restores antioxidant levels, improves mitochondrial activity, and raises ATP levels in the diabetic brain, suggesting they could be a helpful treatment for brain-related complications of diabetes.

Article Abstract

Diabetes exacerbates neuronal injury induced by hyperglycemia mediated oxidative damage and mitochondrial dysfunction. The aim of the present study is to investigate the effects of curcuminoids, polyphenols of Curcuma longa (L.) on oxidative stress and mitochondrial impairment in the brain of streptozotocin (STZ)-induced diabetic rats. A marked increase in lipid peroxidation and nitrite levels with simultaneous decrease in endogenous antioxidant marker enzymes was observed in the diabetic rat brain, which was restored to normal levels on curcuminoids treatment. Down-regulation of mitochondrial complex I and IV activity caused by STZ induction was also up-regulated on oral administration of curcuminoids. Moreover, curcuminoids administration profoundly elevated the ATP level, which was earlier reduced in the diabetic brain. These results suggest that curcuminoids exhibit a protective effect by accelerating antioxidant defense mechanisms and attenuating mitochondrial dysfunction in the brain of diabetic rats. Curcuminoids thus may be used as a promising therapeutic agent in preventing and/or delaying the progression of diabetic complications in the brain.

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Source
http://dx.doi.org/10.1080/10715760802571988DOI Listing

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