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Background and Objective: Oxidative stress is known as the one of the causes of neuropathic pain, reactive oxygen species (ROS) has been reported to be involved in this process. Coenzyme Q10 acts as an antioxidant and is able to reduce resulting oxidative damage. This study was done to determine the effect of Coenzyme Q10 on neuropathic pain in CCI (Chronic Crash Injury) rat model. Materials and Methods: In this experimental study 30 male rats (200-250g) randomizely allocated into 3 groups each 10 rat including CCI, CCI + CoQ10 and CCI + vehicle. Neuropathic pain, was induced by Chronic Crash Injury (CCI) model for sciatic nerve. IP injection of CoQ10 (200 mg/kg) or vehicle was done daily for 10 days. Behavioral tests were done before and after surgery on day 5 and 10 respectively. Paw withdrawal threshold was assessed by Randall Selitto test, Analgesy Metter and Von Frey filaments. Data was analyzed by SPSS-14, Independent T and Mean-whatney tests. Results: Induction of nerve injury decreased pain threshold (P

Despite the vast improvements of cell therapy in spinal cord injury treatment, no optimum protocol has been developed for application of neural stem/progenitor cells. In this regard, the present meta-analysis showed that the efficacy of the neural stem/progenitor cell (NSPC) transplantation depends mainly on injury model, intervention phase, transplanted cell count, immunosuppressive use, and probably stem cell source. Improved functional recovery post NSPC transplantation was found to be higher in transection and contusion models. Moreover, NSPC transplantation in acute phase of spinal injury was found to have better functional recovery. Higher doses (>3 × 10 6 cell/kg) were also shown to be optimum for transplantation, but immunosuppressive agent administration negatively affected the motor function recovery. Scaffold use in NSPC transplantation could also effectively raise functional recovery. [ABSTRACT FROM AUTHOR]

Background Patients with chronic pain usually suffer from learning and memory impairment which may significantly decrease their quality of life. Despite laboratory and clinical studies, the mechanism underlying this memory impairment remains elusive. We evaluated the effect of chronic pain on the glutamate and GABA levels and BDNF expression in the CA1 region of hippocampus as a possible explanation for memory impairment related to neuropathic pain. Methods In this respect, 30 male rats were randomly allocated to 3 groups as control, sham and neuropathic. Neuropathic pain was induced by a chronic constriction injury of the sciatic nerve (CCI) and mechanical allodynia and the spatial memory was assessed using the Von Frey filaments and Morris water maze respectively. To determine the potential mechanisms, the in vivo extracellular levels of glutamate and γ-aminobutyric acid (GABA) were measured by microdialysis and the brain-derived neurotrophic factor (BDNF) expression was determined by using western blots technique in the hippocampus on days 14 and 21 post-CCI. Results We showed that CCI impaired spatial learning and memory in Morris water maze (MWM) task. BDNF expression level and glutamate concentration significantly decreased in rats with chronic constriction injury of the sciatic nerve (P < 0.001, F = 7.3, F = 23.23). In addition, GABA increased in hippocampal CA1 region (P < 0.001, F = 39.2) when the pain threshold was minimum. Nevertheless, these changes reversed while pain was relieved spontaneously. Conclusion Chronic pain induced by constriction of the sciatic nerve impairs the spatial learning and memory function in rats. This effect exerts through the increase in GABA concentration and decrease in the glutamate and BDNF levels in the CA1 region of the hippocampus. [ABSTRACT FROM AUTHOR]