Neuroprotective effects of allicin on spinal cord ischemia-reperfusion injury via improvement of mitochondrial function in rabbits.

Allicin, the active substance of garlic, exerts a broad spectrum of pharmacological activities and is considered to have potential therapeutic applications. The present study was designed to investigate the beneficial effects of allicin against spinal cord ischemia-reperfusion (I/R) injury and its associated mechanisms. Male New Zealand white rabbits were pretreated with allicin (1, 10 and 50 mg/kg) for two weeks, and exposed to infrarenal aortic occlusion-induced spinal cord I/R injury. We found that allicin significantly reduced the volume of the spinal cord infarctions, improved the histopathologic features and increased the number of motor neurons in a dose-dependent manner. This protection was associated with an improvement in neurological function, which was measured by the hind-limb motor function scores. Furthermore, allicin also significantly suppressed the accumulations of protein and lipid peroxidation products, and increased the activities of endogenous antioxidant enzymes, including catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX) and glutathione S-transferase (GST). In addition, allicin treatment preserved the function of mitochondria respiratory chain complexes and inhibited the production of ROS and the release of mitochondrial cytochrome c in the spinal cord of this model. Collectively, these findings demonstrated that allicin exerts neuroprotection against spinal cord I/R injury in rabbits, which may be associated with the improvement of mitochondrial function.