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出 处:《中华麻醉学杂志》2011年第5期613-615,共3页Chinese Journal of Anesthesiology
摘 要:目的 探讨七氟醚预处理对局灶性脑缺血再灌注损伤大鼠皮质C/EBP同源蛋白(CHOP)表达的影响。方法健康雄性SD大鼠36只,体重250—280g,采用随机数字表法,将大鼠随机分为3组(n=12):假手术组(S组)、局灶性脑缺血再灌注组(I/R组)和七氟醚预处理组(Sevopc组)。采用线栓法阻断右侧大脑中动脉1h,再灌注24h,制备局灶性脑缺血再灌注损伤模型。Sevo-pc组于缺血前1h吸入2.7%七氟醚。各组=F再灌注24h时行神经功能缺陷评分后断头取脑,TIC染色法测定脑梗死体积,免疫组化法测定缺血侧皮质CHOP表达,TUNEL法计数凋亡神经细胞。结果与S组比较,I/R组和Sevo-pc组神经功能缺陷评分升高,脑梗死体积比升高,缺血侧皮质CHOP表达上调,凋亡细胞数增加(P〈0.01);与I/R组比较,Sevo-pc组神经功能缺陷评分降低,脑梗死体积比降低,缺血侧皮质CHOP表达F调,凋亡细胞数喊少(P〈0.05或0.01)。结论七氟醚预处理可能通过下调皮质CHOP表达减轻大鼠局灶性脑缺血再灌注损伤。Objective To investigate the effect of sevoflurane preconditioning on CCAAT/enhancer binding protein (C/EBP) homologous protein (CHOP) expression in the cerebral cortex after focal cerebral ischemiareperfusion (I/R) injury in rats and the mechanism. Methods Thirtysix male SD rats weighing 250-280 g were randomly divided into 3 groups (n = 12 each) : sham operation group (group S), focal cerebral I/R group (group I/R) and sevoflurane preconditioning group (group Sevo-pc). The animals were anesthetized with intraperitoneal chloral hydrate 300 mg/kg. In groups I/R and Sevo-pc, focal cerebral ischemia was induced by middle cerebral ar- tery occlusion using a nylon thread with roundel tip inserted into the right internal carotid artery and advanced cranially until resistance was met. The occlusion was maintained for 1 h followed by 24 h reperfusion. Group Sevo-pc inhaled 2.7% sevoflurane for 1 h before ischemia. Neurological deficits were assessed and scored at the end of 24 h reperfiasion and then the rats were decapitate, t. Their brains were immediately removed. The cerebral infarct size was determined by TTC staining. The CHOP expression in the iscbemic cerebral cortex was determined by immunohistochemistry. The number of apoptotic neurons was counted using TUNEL. Results The neurological deficit scores were significantly higher, the cerebral infarct size was significantly larger, and the CHOP expression and the number of apoptotic neurons were significantly higher in groups I/R and Sevo-pc than in group S ( P 〈 0.01 ). The neurological deficit scores were significantly lower, the cerebral infarct size was significantly smaller, and the CHOP expression and the number of apoptosis neurons were significantly lower in group Sevo-pc than in group I/R ( P 〈 0.05 or 0.01 ). Conclusion Sevoflttranc preconditioning may protect the brain against focal cerebral I/R injury by down-regulating CHOP expression in the cerebral cortex in rats.
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