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目的观察γ-氨基丁酸(GABA)受体阻滞剂普瑞巴林(PGB)对癫痫大鼠的干预作用及其作用机制。方法按随机数字表法将38只健康成年SD大鼠分为对照组,戊四氮(PTZ)组,PGB低、中、高剂量组。按Racine分级方法观察癫痫大鼠行为学表现,同时描记脑电图变化;通过苏木素-伊红染色法观察海马神经元的形态学改变,采用免疫组织化学法检测海马组织p38MAPK的蛋白表达。结果与对照组比较,PTZ组大鼠癫痫发作级别明显增高,表现为Ⅳ~Ⅴ级发作(P<0.01),海马组织中p38MAPK的蛋白表达增强(P<0.01);与PTZ组比较,PGB组大鼠癫痫发作级别明显降低,表现为Ⅰ~Ⅲ级发作(P<0.01),海马组织中p38MAPK的蛋白表达减弱(P<0.05);PGB组间比较,高、中剂量组大鼠癫痫发作级别较低剂量组降低(P<0.05),海马组织中p38MAPK的蛋白表达较低剂量组减弱(P<0.05)。结论 p38MAPK通路在PTZ诱导的癫痫大鼠海马中表达增强,GABA受体阻滞剂PGB对癫痫大鼠具有保护作用,其作用是通过间接下调p38MAPK的蛋白表达实现的。
Objective To observe the effect of GABA receptor blocker pregabalin (PGB) on epilepsy rats and its mechanism. Methods Thirty-eight healthy adult SD rats were randomly divided into control group, pentylenetetrazole (PTZ) group, PGB low, medium and high dose groups. The morphological changes of hippocampal neurons were observed by hematoxylin-eosin staining and the protein expression of p38MAPK in hippocampus was detected by immunohistochemical method. Results Compared with the control group, the level of seizure in PTZ group was significantly increased (P <0.01), and the expression of p38MAPK in hippocampus was increased (P <0.01). Compared with PTZ group, PGB group The level of epileptic seizures in rats was significantly lower (P <0.01), and the protein expression of p38MAPK in hippocampus decreased (P <0.05). The level of seizure Compared with the lower dose group (P <0.05), the protein expression of p38MAPK in the hippocampus was weaker than the lower dose group (P <0.05). Conclusion p38MAPK pathway is enhanced in hippocampus of PTZ-induced epilepsy rats, and PGB of GABA receptor antagonist has a protective effect on epileptic rats. The effect of p38MAPK pathway is indirectly through down-regulating the protein expression of p38MAPK.