【摘要】：目的觀察絲裂原活化蛋白激酶(MAPKs)阻滯劑U0126對創(chuàng)傷性腦損傷(TBI)大鼠學(xué)習(xí)記憶功能的影響,并探討其機制。方法將313只成年雄性SD大鼠隨機分為假手術(shù)組52只、模型組87只、DMSO組87只、U0126組87只,除假手術(shù)組外其余各組制備大鼠彌漫性腦創(chuàng)傷模型。U0126組將0.1 mg/kg U0126以0.1 mmol/L的PBS稀釋至300μL,于造模前30 min尾靜脈注射。DMSO組同時點尾靜脈注射相同含量DMSO稀釋溶液,假手術(shù)組和模型組同時點尾靜脈注射生理鹽水300μL。造模30 min、3 h、12 h、24 h、48 h、72 h、7 d取各組大鼠各5只(假手術(shù)組3只),采用TUNEL法觀察各組海馬組織神經(jīng)細胞凋亡情況。造模30 min、3 h、12 h、24 h、48 h、72 h、7 d取各組大鼠各6只(假手術(shù)組3只),采用Western blot法檢測各組海馬組織磷酸化細胞外信號調(diào)節(jié)激酶1/2(p-ERK1/2)蛋白表達。造模14、16、18、21 d取各組大鼠各10只,采用Morris水迷宮實驗觀察大鼠空間學(xué)習(xí)記憶能力。結(jié)果造模48、72 h時,U0126組海馬組織神經(jīng)細胞凋亡數(shù)少于DMSO組、模型組,P均0.05;造模24、48、72 h時,U0126組、DMSO組、模型組海馬組織神經(jīng)細胞凋亡數(shù)均多于假手術(shù)組,P均0.05;造模48、72 h時,U0126組海馬組織p-ERK1/2蛋白相對表達量低于模型組、DMSO組,P均0.05;造模12、24、48、72 h時,U0126組、DMSO組、模型組海馬組織p-ERK1/2蛋白相對表達量均短于假手術(shù)組,P均0.05;造模16、18、21 d時U0126組大鼠潛伏期均短于DMSO組、模型組,P均0.05;造模14、16、18、21 d時U0126組、DMSO組、模型組大鼠潛伏期均長于假手術(shù)組,P均0.05。相關(guān)性分析結(jié)果顯示,海馬區(qū)神經(jīng)細胞凋亡數(shù)與p-ERK1/2表達呈正相關(guān)(r=0.468,P=0.002)。結(jié)論 U0126可抑制TBI大鼠海馬神經(jīng)細胞凋亡,提高大鼠的學(xué)習(xí)記憶能力,可能與降低海馬組織中pERK1/2表達有關(guān)。
[Abstract]:Objective to investigate the effects of U0126, a mitogen-activated protein kinase (MAPKs) blocker, on learning and memory function in (TBI) rats with traumatic brain injury. Methods 313 adult male SD rats were randomly divided into sham-operated group (n = 52), model group (n = 87), DMSO group (n = 87) and U0126 group (n = 87). The model of diffuse brain trauma was established in rats in each group except sham-operation group. Group U0126 diluted 0.1 mg/kg U0126 to 300 渭 L with 0.1 mmol/L PBS. 30 min before the model, the DMSO group was injected with the same amount of DMSO diluted solution, and the sham operation group and the model group were injected with 300 渭 L saline simultaneously. The apoptosis of hippocampal nerve cells in each group was observed by TUNEL method. Five rats in each group (3 rats in sham-operation group) were taken from each group for 7 days after 30 min,3 / 12 h and 48 h / 48 h and 72 h / d respectively. The apoptosis of hippocampal nerve cells in each group was observed by TUNEL method. Six rats in each group (3 rats in sham-operation group) were taken for 7 days. The expression of extracellular signal regulated kinase 1 / 2 (p-ERK1/2) protein in hippocampal tissue was detected by Western blot assay. The spatial learning and memory ability of rats in each group was observed by Morris water maze experiment. Results the number of neuronal apoptosis in hippocampal tissue of U0126 group was lower than that of DMSO group (P 0.05), and that of U0126 group, DMSO group and model group was more than that of sham operation group (P 0.05). The relative expression of p-ERK1/2 protein in hippocampal tissue of U0126 group was lower than that of model group and DMSO group (P 0.05). The relative expression of p-ERK1/2 protein in hippocampal tissue of U0126 group, DMSO group and model group was shorter than that of sham operation group (P 0.05), and the latency of U0126 group was shorter than that of DMSO group (P 0.05). The latencies of U0126 group, DMSO group and model group were longer than those of sham operation group (P 0.05). The results of correlation analysis showed that the number of neuronal apoptosis in hippocampus was positively correlated with the expression of p-ERK1/2 (r 0. 468 P0. 002). Conclusion U0126 can inhibit the apoptosis of hippocampal neurons and improve the learning and memory ability of TBI rats, which may be related to the decrease of pERK1/2 expression in hippocampus.
【作者單位】： 唐山市工人醫(yī)院;華北理工大學(xué)基礎(chǔ)醫(yī)學(xué)院;
【基金】：河北省自然科學(xué)基金資助項目(H2012401071) 河北省引進留學(xué)人員資助項目(2012-02)
【分類號】：R651.15

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