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作 者:郭建荣[1] 崔健君[1] 陈卫民[1] 孟凌新[1] 高红[2]
机构地区:[1]中国医科大学附属第二医院麻醉科,沈阳市110004 [2]中国医科大学卫生部小儿先天畸形重点实验室,沈阳市110004
出 处:《中华麻醉学杂志》2003年第3期204-206,共3页Chinese Journal of Anesthesiology
摘 要:目的观察异丙酚对氯胺酮诱导的热休克蛋白70(HSP70)基因在大鼠后扣带回皮质区表达的影响,探讨异丙酚抑制氯胺酮所致精神症状和神经损害的机制。方法 雄性Wistar大鼠30只,随机分为生理盐水5 ml组、氯胺酮100 mg/kg组、异丙酚100 mg/kg组、异丙酚50 mg/kg-氯胺酮100mg/kg组、异丙酚100 mg/kg-氯胺酮100 mg/kg组。于用药后24 h,大鼠断头取脑,用半定量RT-PCR技术和免疫组织化学方法检测各组HSP70 mRNA和HSP 70蛋白在大鼠后扣带回皮质区的表达。结果 氯胺酮可明显诱导HSP70 mRNA与HSP70蛋白在大鼠后扣带回皮质区的表达;异丙酚自身不能诱导HSP70基因的表达;预先给予异丙酚可显著抑制氯胺酮诱导的HSP70 mRNA和HSP70蛋白在这一区域的表达,且抑制效应呈剂量依赖性。结论异丙酚可抑制氯胺酮诱导的HSP 70 mRNA与HSP70蛋白在大鼠后扣带回皮质区的表达,这可能是其预防或减轻氯胺酮所致精神症状和神经损害的机制之一。Objective To investigate the effects of propofol on ketamine-induced HSP 70 mRNA and protein expression in the rat posterior cingulate cortex and to explore the possibility of using propofol to prevent or treat ketamine-induced psychotomimetic effects and neuronal damage. Methods Thirty male Wistar rats weighing 250-300 g were randomly divided into 5 groups with 6 animals in each group: group 1 received normal saline intraperitoneally ip (NS); group 2 received ketamine 100 mg· kg-1 ip (K); group 3 received propofol 100 mg · kg-1 ip (P); group 4 received propofol 50 mg·kg-1 + ketamine 100 mg·kg-1 ip (P1 K) and group 5 received propofol 100 mg·kg + ketamine 100 mg·kg-1 ip (P2K) . In group 4 and 5 the interval between propofol and ketamine administration was 15 min. Twenty-four hours after ketamine and/or propofol administration, the animals were decapitated and brain was removed. HSP 70 mRNA expression in the posterior cingulate cortex was detected by using semi-quantitative RT-PCR technique; HSP 70 protein expression in posterior cingulated cortex was determined by immuno-histochemical method. Results The levels of HSP 70 mRNA and HSP 70 protein expression were significantly different among the 5 groups. Ketamine induced marked HSP 70 mRNA and HSP 70 protein expression in the posterior cingulated cortex. Propofol itself did not induce HSP 70 gene expression in this brain region. Propofol significantly inhibited ketamine-induced HSP 70 mRNA and HSP 70 protein expression in the posterior cingulate cortex in a dose-dependent manner. Conclusions Propofol pretreatment can significantly inhibit ketamine-induced HSP 70 mRNA and protein expression in the posterior cingulated cortex. It may be one of the mechanisms of inhibition of ketamine-induced psychotomimetic effect and neuronal damage by propofol.
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