An Experimental Study Of Celecoxib On Neuronal Apoptosis In The Hippocampus Induced By Status Epilepiticus

Objective: Status epilepticus(SE) is one of the medical emergency which can cause acute and permanent central neural system damage, especially neuronal damage of limbic system such as hippocampus. It can promote the formation and development of seizures,and at last result in brain dysfunction. Apoptotic neuronal cell death is one of the forms of neuronal cell death after SE. Recent study found that,cox-2 inhibitor has a neuroprotective effect, but little research in epilepsy.In this study,we evaluated the neuroprotective effects and the possible mechanism of celecoxib on the neuronal apoptosis in rat brain by acute seizures.so as to provide a new method or way for the protection of brain damage after SE.Methods: Seizures were induced in fifty-four adult rats(ARs) with lithium and pilocarpine injected intraperitoneally. 54 male Wistar rats were randomly divided into three groups:Group Li-Pilo, Group celecoxib and the control group. Using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) observed 12 h after SE, 24h, 72h and 7d hippocampal neuronal apoptosis dynamic changes, and the immunohistochemical staining was used to examine the expression of bcl-2 protein.Results: In the control group, TUNEL-positive cells can not be found in hippocampus. In group Li-Pi ,The number of apoptotic neurons in the hippocampus increased significantly 12 h after SE. The number of apoptotic neuron peaked at 72 h,significantly decreased at 7 day.The number of apoptotic neurons of celecoxib group at each different time points were significantly less than the Li-Pilo group (P<0.01). bcl-2 immunohistochemical staining:bcl-2 was slightly expressed in control group. In Group Li-Pilo, there was comparatively apparent expression at 12h. The expression began to decrease at 24h, and only little could be seen at 72h. As for Group celecoxib, the expression was apparent 12 h after SE, became strong at 24h and remained till 72h.Conclusion: Pretreatment of celecoxib could increase the expression of bcl-2, which might be the mechanism of its protective effect for neurons.