【摘要】：目的觀察干預(yù)癲癇大鼠自噬活性對(duì)小膠質(zhì)細(xì)胞激活狀態(tài)及分泌腫瘤壞死因子-α(TNF-α)水平變化的影響,探討其對(duì)神經(jīng)元以及癲癇狀態(tài)的影響。方法 Wistar大鼠隨機(jī)分為正常對(duì)照組(6只)與癲癇組(24只);癲癇組大鼠采用戊四氮制作癲癇模型,造模成功后隨機(jī)分為致癇對(duì)照組、3-甲基嘌呤(3-MA)組及雷帕霉素(RAPA)組,每組各6只。觀察記錄各組大鼠行為學(xué)及腦電圖變化,采用HE及Nissl染色觀察CA1區(qū)神經(jīng)元損傷情況,免疫熒光染色及Western blot檢測(cè)海馬組織LC3、CD68及TNF-α的表達(dá)。結(jié)果致癇對(duì)照組顯示癲癇可導(dǎo)致神經(jīng)元損傷,LC3、CD68、TNF-α的表達(dá)較正常對(duì)照組顯著增加(P0.05)。3-MA組與致癇對(duì)照組相比癲癇發(fā)作等級(jí)降低;神經(jīng)元損傷數(shù)目減少;LC3、CD68、TNF-α的表達(dá)顯著降低(P0.05)。RAPA組大鼠癲癇發(fā)作等級(jí)、CD68和TNF-α的表達(dá)較致癇對(duì)照組無(wú)明顯變化(P0.05);但神經(jīng)元損傷數(shù)目及LC3的表達(dá)進(jìn)一步增加(P0.05)。結(jié)論癲癇過(guò)程中存在自噬現(xiàn)象,其可激活小膠質(zhì)細(xì)胞,促進(jìn)TNF-α分泌,導(dǎo)致神經(jīng)元損傷;而抑制自噬活性可調(diào)控小膠質(zhì)細(xì)胞,減少TNF-α的分泌,保護(hù)神經(jīng)元,從而減輕癲癇發(fā)作狀態(tài)。
[Abstract]:Objective to observe the effects of autophagy on the activation of microglia and the secretion of tumor necrosis factor- 偽 (TNF- 偽) in epileptic rats. Methods Wistar rats were randomly divided into normal control group (n = 6) and epilepsy group (n = 24). The epileptic rats in the epileptic group were randomly divided into three groups: epileptogenic control group, 3-methylpurine (3-MA) group and rapamycin (RAPA) group, with 6 rats in each group. The changes of ethology and electroencephalogram (EEG) in each group were observed. The neuronal damage in CA1 area was observed by HE and Nissl staining. The expression of LC3,CD68 and TNF- 偽 in hippocampus was detected by immunofluorescence staining and Western blot. Results Epilepsy control group showed that epilepsy could cause neuronal injury, and the expression of LC3,CD68,TNF- 偽 was significantly higher than that of normal control group (P0.05). The grade of epileptic seizure and the number of neuron damage in 3-MA group were lower than those in epileptic control group. The expression of LC3,CD68,TNF- 偽 was significantly decreased (P0.05) in the). RAPA group, but the expression of CD68 and TNF- 偽 was not significantly changed compared with the epileptic control group (P0.05). However, the number of neuronal injury and the expression of LC3 were further increased (P0.05). Conclusion there is autophagy in the course of epilepsy, which can activate microglia, promote the secretion of TNF- 偽, and lead to neuronal injury. Inhibition of autophagy can regulate microglia, reduce the secretion of TNF- 偽, protect neurons and relieve epileptic seizures.
【作者單位】： 濱州醫(yī)學(xué)院附屬醫(yī)院;濱州醫(yī)學(xué)院;
【分類號(hào)】：R742.1

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