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目的:探讨抑制p38MAPK通路对减轻红藻氨酸诱导的颞叶癫痫发作引起大鼠海马神经元所造成损害的作用和机制。方法:经侧脑室给予不同剂量(0,0.01,0.1,1μg)SB203580(p38MAPK特异性抑制剂)预处理,30min后再予红藻氨酸制作大鼠颞叶癫痫持续状态模型。7d后采用Nissl染色方法观察海马各区的锥体细胞和颗粒细胞的情况。结果:红藻氨酸注射7d后CA3区可见大量锥体细胞缺失,尚存细胞变性,伴局限性颗粒细胞增多,呈放射状分布。CA1区受累较轻,但也存在一定程度的细胞脱失。预先给予SB203580(0.1μg以上剂量)处理的动物以上变化明显减轻。假手术大鼠海马各区有大量正常致密锥体细胞,未见细胞脱失。结论:大鼠侧脑室内注射红藻氨酸引起全身痉挛性癫痫持续状态对海马神经元造成损害,而抑制p38MAPK通路,对海马神经元起一定保护作用。
OBJECTIVE: To investigate the effect and mechanism of inhibition of p38 MAPK pathway on the lesion of rat hippocampal neurons induced by kainic acid induced temporal lobe epilepsy. Methods: After pretreatment with SB203580 (specific inhibitor of p38MAPK) at different doses (0, 0.01, 0.1, 1μg) in the lateral ventricle, the rat model of temporal lobe epilepsy was established after 30min. After 7 days Nissl staining was used to observe the pyramidal cells and granulosa cells in the hippocampus. Results: After 7 days of injection of kainic acid, a large number of pyramidal cells were found in CA3 area, while the surviving cells were degenerated with the increase of confined granulosa cells in radial distribution. CA1 area involved less, but there is also a certain degree of cell loss. The above changes of animals pretreated with SB203580 (above 0.1μg dose) were significantly reduced. There was a large number of normal dense pyramidal cells in the hippocampus in sham-operated rats, and no cell loss occurred. CONCLUSION: The intracerebroventricular (icv) injection of kainic acid causes the generalized convulsive status epilepticus to damage the hippocampal neurons and inhibit the p38MAPK pathway, which may play a protective role in hippocampal neurons.