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首页> 外文期刊>The European Journal of Neuroscience >The selective cyclooxygenase-2 inhibitor rofecoxib reduces kainate-induced cell death in the rat hippocampus.
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The selective cyclooxygenase-2 inhibitor rofecoxib reduces kainate-induced cell death in the rat hippocampus.

机译：选择性环氧合酶2抑制剂rofecoxib减少了海马因海因酸盐诱导的细胞死亡。

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摘要

Treatment of male Sprague-Dawley rats with kainic acid (10 mg/kg, i.p.) triggered limbic seizures in 60% of the animals starting within 30 min and lasting for about 6 h. Cyclooxygenase-2 (COX-2) mRNA was strongly induced in the pyramidal cells of the hippocampus, in the amygdala and the piriform cortex after 8 h, as shown by in situ hybridization, and returned to control levels after 72 h. At this time marked cell loss occurred in the CA1-CA3 areas of the hippocampus. We hypothesize that rofecoxib, a selective COX-2 inhibitor, might abbreviate the late neurotoxicity, possibly associated with COX-2 induction. Animals which developed seizures were treated for 3 days with rofecoxib (10 mg/kg, i.p., n = 12) starting 6 or 8 h after kainic acid injection. Histological staining of viable cells confirmed that rofecoxib treatment selectively diminished cell loss in the hippocampus. The TdT-mediated dUTP nick end labelling (TUNEL) technique was used to estimate delayed cell death. Abundant TUNEL-positive cells were detected in seizure rats 72 h after kainic acid injection in pyramidal cells of the hippocampus (CA1-CA3), in cells of the thalamus, the amygdala and the piriform cortex. Treatment with rofecoxib selectively and significantly (P < 0.05) attenuated the number of TUNEL-positive cells in the hippocampus, whereas the cells of the thalamus, amygdala and piriform cortex were not protected. Therefore we conclude that COX-2 might contribute to cell death of pyramidal cells of the hippocampus as a consequence of limbic seizures.
机译：用海藻酸（10 mg / kg，腹腔注射）治疗雄性Sprague-Dawley大鼠，在30分钟内触发了60％动物的边缘性癫痫发作，持续约6小时。原位杂交显示，环氧合酶2（COX-2）mRNA在海马锥体细胞，杏仁核和梨状皮质中强烈诱导8 h，如原位杂交所示，在72 h后恢复至对照水平。此时，在海马CA1-CA3区发生明显的细胞丢失。我们假设罗非考昔（一种选择性的COX-2抑制剂）可能会简化晚期神经毒性，可能与COX-2诱导有关。注射海藻酸后6或8小时，用罗非考昔（10 mg / kg，i.p.，n = 12）治疗癫痫发作的动物3天。活细胞的组织学染色证实罗非昔布治疗选择性地减少了海马细胞的丢失。 TdT介导的dUTP缺口末端标记（TUNEL）技术用于估计延迟的细胞死亡。在海藻酸注射后72 h，癫痫大鼠海马锥体细胞（CA1-CA3），丘脑，杏仁核和梨状皮层细胞中检测到大量的TUNEL阳性细胞。用罗非考昔选择性且显着（P <0.05）处理可减弱海马中TUNEL阳性细胞的数量，而丘脑，杏仁核和梨状皮质的细胞则不受保护。因此，我们得出结论，由于边缘性癫痫发作，COX-2可能导致海马锥体细胞死亡。

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