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机构地区:[1]223300南京医科大学附属淮安第一医院麻醉科
出 处:《中华麻醉学杂志》2013年第9期1079-1081,共3页Chinese Journal of Anesthesiology
摘 要:目的 评价右美托咪定对利多卡因诱发大鼠皮层神经元凋亡的影响.方法 SD大鼠胎鼠皮层神经元,以1×105个/ml密度接种于24孔培养板(1 ml/孔),80个培养孔,采用随机数字表法,将其分为4组(n=20),正常对照组(C组)常规培养;利多卡因组(L组)培养基中加入利多卡因,终浓度为1 mmol/L;右美托咪定组(D组)培养基中加入右美托咪定,终浓度为3μmol/L;利多卡因+右美托咪定组(L+D组)培养基中加入利多卡因和右美托咪定,终浓度分别为1mmol/L、3μmol/L.孵育4h,行DAPI染色,检测细胞凋亡情况,计算细胞凋亡率,采用免疫印迹法检测磷酸化丝氨酸-苏氨酸激酶(p-Akt)、Akt和caspase-3表达.结果 与C组比较,L组和L+D组皮层神经元凋亡率升高,皮层神经元p-Akt表达下调,caspase-3表达上调(P<0.05),D组上述指标差异无统计学意义(P>0.05);与L组比较,L+D组皮层神经元凋亡率降低,皮层神经元p-Akt表达上调,caspase-3表达下调(P<0.05);4组间皮层神经元Akt表达比较差异无统计学意义(P>0.05).结论 右美托咪定可减轻利多卡因诱发大鼠皮层神经元凋亡,机制与激活Akt有关.Objective To evaluate the effects of dexmedetomidine on lidocaine-induced apoptosis in rat cortical neurons.Methods The cortical neurons obtained from Sprague-Dawley fetal rats were seeded in 24 multiwell plates at a density of 1 × 105 cells/ml,and the cortical neurons of 80 wells were randomly divided into 4 groups (n =20 each):control group (group C),lidocaine group (group L),dexmedetomidine group (group D) and lidocaine + dexmedetomidine group (group L+ D).The cells were cultured routinely in group C.The cells were exposed to lidocaine with a final concentration of 1 mmol/L in group L.The cells were exposed to dexmedetomidine with a final concentration of 3 μmol/L in group D.The cells were exposed to lidocaine and dexmedetomidine with the final concentrations of 1 mmol/L and 3 μmol/L,respectively,in group L + D.After 4 h incubation,the neurons were subjected to DAPI staining for detection of apoptosis,and the apoptosis rate was calculated.Western blot analysis was used to measure the expression of phosphorylated Akt (p-Akt),Akt and caspase-3.Results Compared with group C,the apoptosis rate was significantly increased,the expression of p-Akt was down-regulated,and the expression of caspase-3 was up-regulated in L and L + D groups (P 〈 0.05),while no significant changes were found in the indexes mentioned above in group D (P 〉 0.05).Compared with group L,the apoptosis rate was significantly decreased,the expression of p-Akt was up-regulated,and the expression of caspase-3 was down-regulated in L + D group (P 〈 0.05).There was no significant difference in the expression of Akt between the four groups (P 〉 0.05).Conclusion Dexmedetomidine can reduce lidocaine-induced apoptosis in rat cortical neurons,and activation of Akt may be involved in the underlying mechanism. Keywords:Dexmedetomidine ; Lidocaine ; Apoptosis ; Neurons ; Cerebral cortex
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