CAJ | 학술논문

目的观察戊四氮点燃癫痫持续状态大鼠海马部位细胞外信号调节激酶(extracellular-regulated kinase ERK1/2)的变化规律及尼莫地平对其的影响.方法 7～8周龄清洁级健康雄性Sprague-Dawley (SD)大鼠,用随机数字表法分为3组:正常对照组(normal control,NC)35只、持续癫痫发作组(SE) 40只和尼莫地平干预组(NIM) 40只,采用腹腔注射戊四氮的方法制作癫痫持续状态模型,尼莫地平组大鼠在腹腔注射戊四氮前15 min给予尼莫地平腹腔注射(2.5mg/kg),应用Western Blot的方法检测海马部位ERK的变化规律.结果尼莫地平干预后,大鼠癫痫发作程度减轻,发作持续时间缩短.SE组大鼠海马部位p-ERK1/2表达存在动态变化.尼莫地平组大鼠海马部位P-ERK表达较癫痫组明显升高(3.26±0.95,2.56 ±0.82,P＜0.05).结论 L型钙离子拮抗剂尼莫地平能够减轻戊四氮点燃大鼠的癫痫发作程度,其抗癫痫作用可能与海马部位ERK信号通路有关.
목적 관찰무사담점연전간지속상태대서해마부위세포외신호조절격매(extracellular-regulated kinase ERK1/2)적변화규률급니막지평대기적영향.방법 7～8주령청길급건강웅성Sprague-Dawley (SD)대서,용수궤수자표법분위3조:정상대조조(normal control,NC)35지、지속전간발작조(SE) 40지화니막지평간예조(NIM) 40지,채용복강주사무사담적방법제작전간지속상태모형,니막지평조대서재복강주사무사담전15 min급여니막지평복강주사(2.5mg/kg),응용Western Blot적방법검측해마부위ERK적변화규률.결과 니막지평간예후,대서전간발작정도감경,발작지속시간축단.SE조대서해마부위p-ERK1/2표체존재동태변화.니막지평조대서해마부위P-ERK표체교전간조명현승고(3.26±0.95,2.56 ±0.82,P＜0.05).결론 L형개리자길항제니막지평능구감경무사담점연대서적전간발작정도,기항전간작용가능여해마부위ERK신호통로유관.
Objective To detect the expression of extracellular-regulated kinase (ERK) and phosphatedextracellular-regulated kinase (P-ERK) in the hippocampus after pentylenetetrazoloe-induced status epilepsy and the effects of nimodipine on it.Methods Male Sprague-Dawley adult rats (200-250 g) were randomly divided into normal control group(NC,n =35),status epilepsy group (SE,n =40),nimodipine group (NIM,n =40).The rats were injected first with 40 mg/kg pentylenetetrazoloe(PTZ),followed 10 minutes later by 20 mg/kg PTZ,and subsequently,10 mg/kg PTZ ip every 10 minutes until SE occurred,apoint charactered by a loss of postural control and tonic-clonic seizures.Rats in control group received the same number of saline injections.Rats in NIM group were injected NIM(2.5 mg/kg) intraperitoneally 15 min before the injection of PTZ.Rats in every group were killed at 30 minutes,1 hour,3 hours,12 hours,24 horus,72 hours and 7 days after status epilepsy respectively and the hippocampus were dissected.The expression of ERK and P-ERK in the hippocampus were detected by Western blot.Results Nimodipine attenuated the convulsion of PTZ-induced status epilepsy.There was dynamic expression of P-ERK in SE group.In NIM group,the expression of P-ERK was markedly increased than that of SE group at 30 min,1h,3h,12h,24h,72h,and 7d (3.26 ±0.95 vs 2.56 ±0.82 at 30 min,P＜0.05).Conclusion Nimodipine attenuates the convulsion of PTZ-induced status epilepsy with increased expression of phosphated-ERK in the hippocampus of rats.