The Effect of @entity38001 in @entity9 Induced by Chronic Constriction Injury in XXXX .

@entity1931 @entity1976 @entity2310 @entity16 @entity2041 @entity38001 @entity1234 @entity35 @entity8638 @entity9
UNASSIGNED: We examined the effects of @entity38001 in @entity35 subjected to @entity8638 ( @entity8638 ). @entity38001 (50, 100, and 200   mg/kg, i.p.), was administered from the day of surgery for 14   days. Spinal cord levels of apoptotic factors and glia markers were quantified on days 3, 7, and 14 post- @entity8638 . Oxidative stress markers were assessed on days 7 and 14. @entity8638 @entity35 exhibited a marked mechanical @entity1931 , @entity1931 , and thermal @entity1931 on days 3, 5, 7, 10, and 14 post- @entity8638 . A significant increase in the levels of Iba (a marker of microglia activation) and @entity2310 (a proapoptotic factor) was observed on day 3. Iba remained high on day 7. In contrast, there were no differences in glial fibrillary acidic protein contents between sham and @entity8638 animals. @entity1234 increased and reduced @entity2041 decreased on day 14. @entity38001 significantly attenuated behavioral changes associated with @entity16 . @entity2310 decreased, while @entity1976 was increased by @entity38001 on day 3. @entity38001 also reduced Iba protein on days 3 and 7. The results support evidence that microglial activation, apoptotic factors, and oxidative stress may have a pivotal role in the @entity9 pathogenesis. It is suggested that antinociceptive effects elicited by @entity38001 might be through the inhibition of microglia activation, apoptotic pathways, and antioxidant properties. Copyright    2015 John Wiley _ Sons, Ltd.
