Up-regulated tumor necrosis factor-associated factor 6 level is correlated with apoptosis in the rat cerebral ischemia and reperfusion.

Tumor necrosis-associated factor 6 (TRAF6) performs critical roles in mediating apoptosis-associated inflammatory processes in multiple cell types, but its role in cerebral ischemia-reperfusion (I/R) injury is still unclear. In the present study, we established a middle cerebral artery occlusion (MCAO) reperfusion model in rat, and evaluated both the cerebral inflammatory damage and the cell apoptosis by TTC staining and TUNEL method, respectively. The expression of TRAF6 and the neural cell apoptosis was examined during the I/R pathophysiological process. Cerebral ischemia injury induced significant neuronal cell apoptosis, but after the onset of reperfusion, cell apoptosis was gradually alleviated. In accord with the trend of I/R injury and cell apoptosis, up-regulated TRAF6 mRNA expression and caspase-3 cleavage level were observed in the ischemia stage and the early stage of reperfusion accordingly, which indicated that the activation of TRAF6 correlated positively with the cell apoptosis. Immunohistochemistry staining further showed that the TRAF6 was mainly localized in the neuronal cells. Thus, our study suggested that TRAF6 is involved in the inflammatory process induced by cerebral ischemia-reperfusion, and functions partially as a pro-inflammatory adaptor to mediate cell apoptosis.