Abstract

It is an important therapeutic strategy to protect mitochondria from oxidative stress, especially during ischemia-reperfusion. Curcumin is a naturally occurring phenolic compound isolated as a yellow pigment from turmeric (Curcuma longa). This compound has received much attention due to its diversity of biological and pharmacological activities. In this study, an attempt has been made to evaluate the protective effects of curcumin on rat heart mitochondrial injuries induced by in vitro anoxia-reoxygenation. It was found that curcumin added before anoxia or immediately prior to reoxygenation exhibited remarkable protective effects against anoxia-reoxygenation induced oxidative damage to mitochondria, in concentrations ranging from picomoles to micromoles, with EC50s in the nanomolar range. The protective effects include inhibition of the decrease of state 3 respiratory activity, the decrease of respiratory control ratio (RCR) and ADP:oxygen (ADP:O) ratio, as well as the increase of state 4 respiratory activity; inhibition of the decrease of the membrane fluidity; inhibition of lipoperoxidation and protein carbonylation; as well as inhibition of the enhanced release of cardiolipin (CL) and cytochrome c (Cyt c). These results demonstrate the superior antioxidative properties of curcumin, and make it a promising candidate for the prevention and (or) therapy for ischemia-reperfusion injuries and the related free radical initiated diseases.

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