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醫(yī)學(xué)論文范文:氧化苦參堿對(duì)癲癇大鼠海馬組織內(nèi)ERK信號(hào)轉(zhuǎn)導(dǎo)通路及NR2B表達(dá)的影響
【摘要】 目的 研究氧化苦參堿(Oxymatrine ,Oxy) 對(duì)青霉素致癇大鼠海馬內(nèi)p-ERK 1/2與NR2B表達(dá)含量的影響,探討其抑制癲癇的可能機(jī)制。方法 78只SD大鼠隨機(jī)分為正常組、青霉素(Penicilin,PEN)致癇組、苯巴比妥鈉(phenobarbital sodium，PBS)陽(yáng)性藥物對(duì)照組和Oxy預(yù)處理組,采用免疫組織化學(xué)SABC法檢測(cè)大鼠海馬內(nèi)p-ERK1/2和NR2B陽(yáng)性神經(jīng)元在不同時(shí)間點(diǎn)的表達(dá)。結(jié)果 與青霉素模型組比較，Oxy組1.5h大鼠海馬內(nèi)p-ERK 1/2與NR2B 6.0h組陽(yáng)性細(xì)胞數(shù)減少( P< 0.01) 。結(jié)論 Oxy 拮抗癲癇發(fā)作的機(jī)制可能與調(diào)節(jié)癲癇大鼠腦內(nèi)的p-ERK 1/2水平進(jìn)而使NR2B的水平降低有關(guān)。
【關(guān)鍵詞】 氧化苦參堿;癲癇;p-ERK 1/2;NR2B
Effect on ERK signal transduction pathway in hippocampus
of epileptic rats induced by penicillin
ZHAO Yan, ZHANG Lin-na, CHEN Xiao-xia, et al.(Ningxia Medical University, Yinchuan 750004, China)
[Abstract] Objective To investigate the expression of NR2B and extra cellular signal regulated protein kinase (ERK) signal transduction pathway and the significance in the hippocampus of rats after epileptic seizures induced by PEN (penicillin).Methods 78 healthy SD rats were randomly divided into the normal group, a group induced epilepsy by PEN, a group treated by PBS (Phenobarbital sodium) and a group treated by OXY (Oxymatrine). PEN was intraperitoneally injected and established rat's model of epilepsy. Immunohistochemistry method was used to evaluate p-ERK1 / 2 and NR2B protein expression level changes in hippocampus at different time points. Results In the hippocampus of normal group, no immunoreactivity was detected in p-ERK1/2 and a few immunoreactivity of NR2B was observed. Compared with the PEN group, both the p-ERK 1/2 at 1.5h and NR2B at 6.0h express less in hippocampus in OXY group.Conclusion Following PEN -induced seizure, the activations of ERK in rats in the hippocampus changed at different time points. It is possible that OXY inhibit ERK signal pathway thus reduced the expression of NR2B. Therefore OXY changes the process of pathologic and physiologic reactions in PEN-induced epileptic seizure醫(yī).學(xué)全.在.線網(wǎng)站f1411.cn.
[Key words] Epilepsy; ERK signal transduction pathway; NR2B; Oxymatrine
