本文選題：麻醉藥　切入點：異氟醚后處理　出處：《中國現(xiàn)代醫(yī)學雜志》2017年21期 　論文類型：期刊論文

【摘要】：目的探討異氟醚后處理大鼠海馬腦片缺氧無糖(OGD)損傷神經(jīng)保護機制中細胞外信號蛋白調(diào)節(jié)激酶5(ERK5)的作用。方法使用雄性SD大鼠,將其麻醉后取出海馬組織,制成離體腦片,然后隨機進行正常對照組(Con組)、損傷組(OGD組)和藥物處理組的處理。采用花粉活力染色(TTC)法評價各組腦片損傷程度,采用碘化丙啶(PI)染色法檢測海馬CA1區(qū)神經(jīng)細胞凋亡程度,采用實時熒光定量聚合酶鏈反應(q RT-PCR)測定細胞外調(diào)節(jié)蛋白激酶信使核糖核酸(ERK5 m RNA)的表達,采用Western blot法檢測ERK5蛋白的表達與磷酸化水平。結(jié)果與Con組比較,OGD組腦片損傷程度升高、海馬CA1區(qū)凋亡細胞增多,海馬組織內(nèi)ERK5 m RNA和p-ERK5表達升高(P0.05);XMD組阻斷ERK5 m RNA和p-ERK5表達,腦片損傷程度升高、海馬CA1區(qū)凋亡細胞增多(P0.05)。與OGD、1.5%ISPOC和4.5%ISPOC組比較,3.0%ISPOC組腦片損傷程度減輕、海馬CA1區(qū)凋亡細胞減少,海馬組織內(nèi)ER K5 m R N A和p-ER K5表達升高(P0.05)。與3.0%ISPO C組比較,XMD阻斷ISPOC海馬組織內(nèi)ERK5 m RNA和p-ERK5表達,腦片損傷程度升高、海馬CA1區(qū)凋亡細胞增多(P0.05)。結(jié)論一定濃度的異氟醚后處理大鼠海馬腦片對抗O GD損傷的保護性機制可能與上調(diào)ER K5 m R N A和ERK5磷酸化水平有關。
[Abstract]:Objective to investigate the role of extracellular signal protein regulated kinase (ERK5) in the neuroprotective mechanism of hypoxia-free OGD in rat hippocampal slices treated with isoflurane. Methods male SD rats were anesthetized and the hippocampal tissue was taken out and made into isolated brain slices. Then the normal control group (Con group), the injured group (OGD group) and the drug treated group were randomly treated. The degree of injury of brain slices was evaluated by pollen vigor staining method, and the degree of neuronal apoptosis in the hippocampal CA1 area was detected by the method of pyridine iodide staining. The expression of ERK5 mRNA in extracellular regulated protein kinase messenger ribonucleic acid (ERK5) was detected by real-time fluorescence quantitative polymerase chain reaction (RT-PCR). Results compared with Con group, ERK5 protein expression and phosphorylation level were detected by Western blot. Results compared with Con group, the degree of brain slice damage and apoptosis in the CA1 area of hippocampus were increased, and the expression of ERK5 m RNA and p-ERK5 in hippocampus was increased. The expression of ERK5 m RNA and p-ERK5 was blocked in the Con group. The degree of brain slice injury was increased, and the apoptotic cells in hippocampal CA1 area were increased. Compared with OGD1.5 and 4.5 ISPOC groups, the degree of brain slice damage was reduced and the apoptotic cells in hippocampal CA1 area decreased. The expression of ERK5 m RNA and p-ERK5 increased in hippocampus. Compared with 3.0 ISPO C group, XMD blocked the expression of ERK5 m RNA and p-ERK5 in ISPOC hippocampus. Conclusion the protective mechanism of hippocampal slices treated with isoflurane may be related to the up-regulation of ERK5 mRNA and ERK5 phosphorylation.
【作者單位】： 石河子大學醫(yī)學院第一附屬醫(yī)院麻醉科;石河子大學醫(yī)學院生理教研室;
【基金】：國家自然科學基金(No:81360203)
【分類號】：R614

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