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銀杏葉提取物對紅藻氨酸致癲癇大鼠γ-氨基丁酸A型受體及N-甲基-D-天冬氨酸受體表達(dá)的影響

發(fā)布時(shí)間:2019-01-07 19:35
【摘要】:目的觀察銀杏葉提取物(Ginkgo biloba extract,GBE)預(yù)處理給藥和急性期給藥對癲癇的干預(yù)效應(yīng)及其NR2A受體及GABAA受體表達(dá)的關(guān)系,以探討GBE的抗癲癇機(jī)制。 方法采用側(cè)腦室注射紅藻氨酸(Kainic acid, KA)建立癲癇動物模型。將108只SD大鼠隨機(jī)分為假手術(shù)組(n=18)、GBE對照組(n=18)、癲癇模型組(n=18)、GBE預(yù)處理組(n=18)、GBE急性給藥1組(n=18)、GBE急性給藥2組(n=18)。各組再分為6h、12h及24h亞組(n=6)。應(yīng)用HE染色觀察海馬組織中神經(jīng)元的細(xì)胞形態(tài)變化,用原位雜交技術(shù)測定海馬組織中NR-2AmRNA及GABA-AR mRNA的表達(dá)變化。 結(jié)果GBE預(yù)處理組和GBE急性給藥1組癲癇發(fā)作級別及神經(jīng)元損害較癲癇模型組降低,且以GBE預(yù)處理組損害減輕更明顯。癲癇模型組3個(gè)亞組的大鼠海馬組織中NR-2AmRNA表達(dá)較假手術(shù)組相對應(yīng)各亞組明顯增多(P0.05);GBE預(yù)處理組及GBE急性給藥1組中3個(gè)亞組大鼠海馬組織中NR-2AmRNA表達(dá)明顯低于癲癇模型組相對應(yīng)各亞組(P0.05),GABA-ARmRNA表達(dá)較癲癇模型組相對應(yīng)各亞組明顯增多(P0.05);GBE預(yù)處理組與急性期給藥1組各亞組相比GABA-ARmRNA的表達(dá)上升(P0.05),,NR-2AmRNA的表達(dá)下降(P0.05);癲癇模型組與GBE對照組各亞組相比相關(guān)指標(biāo)均無統(tǒng)計(jì)學(xué)差異(P0.05);急性給藥模型2組3個(gè)亞組的大鼠海馬組織中NR-2AmRNA的表達(dá)較急性模型1組相相對應(yīng)各亞組下降。同組內(nèi)6h、12h、24h三個(gè)時(shí)間點(diǎn)NR-2AmRNA表達(dá)呈下降趨勢,而GABA-ARmRNA表達(dá)則呈上升趨勢。 結(jié)論: GBE干預(yù)有一定的抗癲癇作用,且預(yù)處理給藥比急性期給藥效果更好;其抗癲癇的機(jī)制與減輕神經(jīng)元的損害、減輕癲癇發(fā)作程度、降低NR-2AmRNA的表達(dá)及上調(diào)GABA-ARmRNA的表達(dá)有關(guān)。
[Abstract]:Objective to investigate the effects of (Ginkgo biloba extract,GBE preconditioning and acute administration on epilepsy and the expression of NR2A receptor and GABAA receptor in order to explore the antiepileptic mechanism of GBE. Methods epileptic animal model was established by intracerebroventricular injection of kainic acid (Kainic acid, KA). 108 SD rats were randomly divided into sham operation group (n = 18), GBE control group) and epileptic model group (n = 18), GBE pretreatment group). Each group was subdivided into 6 h, 12 h and 24 h subgroups (nong6). The morphological changes of neurons in hippocampus were observed by HE staining and the expression of NR-2AmRNA and GABA-AR mRNA in hippocampal tissue were detected by in situ hybridization. Results Epilepsy grade and neuronal damage in GBE preconditioning group and GBE acute administration group were lower than those in epileptic model group, especially in GBE preconditioning group. The expression of NR-2AmRNA in hippocampus of the epileptic model group was significantly higher than that of the sham operation group (P0.05). The expression of NR-2AmRNA in hippocampus of GBE preconditioning group and GBE acute administration group was significantly lower than that of epileptic model group (P0.05). The expression of GABA-ARmRNA was significantly higher than that of epileptic model group (P0.05). The expression of GABA-ARmRNA increased and the expression of NR-2AmRNA decreased in GBE preconditioning group compared with that in acute phase group 1 (P0.05). There was no significant difference in the relative indexes between the epileptic model group and the GBE control group (P0.05), and the expression of NR-2AmRNA in hippocampus of the acute model group 2 was lower than that of the acute model group 1. In the same group, the expression of NR-2AmRNA decreased at 6 h, 12 h and 24 h, while the expression of GABA-ARmRNA increased. Conclusion: GBE intervention has some antiepileptic effect, and pretreatment is better than acute administration. Its antiepileptic mechanism is related to the reduction of neuron damage, the reduction of epileptic seizures, the reduction of NR-2AmRNA expression and the up-regulation of GABA-ARmRNA expression.
【學(xué)位授予單位】:桂林醫(yī)學(xué)院
【學(xué)位級別】:碩士
【學(xué)位授予年份】:2014
【分類號】:R742.1


本文編號:2404060

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