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机构地区:[1]中国医科大学附属盛京医院麻醉科,辽宁沈阳110004
出 处:《中国医师杂志》2008年第6期767-770,共4页Journal of Chinese Physician
摘 要:目的通过观察异氟烷预处理在鼠脑缺血再灌注损伤中凋亡相关基因Bcl-2和Bax的mRNA的表达,探讨异氟烷预处理脑保护作用的一氧化氮信号传导通路。方法75只雄性沙士鼠,随机分5组。假手术组(SHAM组):只分离双侧颈总动脉而未子夹闭;缺血再灌注组(I/R组):夹闭双侧颈总动脉5min后开放造成I/R;异氟烷预处理组(ISO组):I/R前60min吸入1.2%~1.5%异氟烷30min;氨基呱(AG)+ISO组:腹腔内注射AG200mg/kg,30min后同ISO组;AG组:I/R前30min注射AG。再灌注24h.取鼠前脑,采用RT-PCR检测脑组织中Bcl-2、Bax基因的mRNA表达。结果ISO组Bcl-2的mRNA表达增高(1.22±0.12).与SHAM组(0.83±0.16)、I/R组(0.83±0.11)和AG+ISO组(0.82±0.12)比较差异有统计学意义(P〈0.05);I/R和AG组BaxmRNA的相对表达量明显增高,与SHAM组比较差异有统计学意义(P〈0.05),ISO组和AG+ISO组表达较弱,但AG+ISO组比ISO组表达略强。结论一氧化氮信号传导通路是异氟烷预处理脑保护作用的途径之一。Objective To investigate the effect of isoflurane preconditioning on Bcl-2 and Bax mRNA expression and the signaling pathway of nitric oxide against brain ischemia-reperfusion (I/R). Methods Seventy-five male gerbils were randomly divided into 5 groups ( n = 15) : SHAM, I/R, ISO, AG + ISO and AG group. Global cerebral I/R was produced by occlusion of bilateral common carotid arteries for 5 minutes and confirmed by isoelectric potential on EEG. In ISO group, the animals inhaled 1.2% - 1.5% isoflurane for 30 minutes followed by 30 minutes wash-out period before I/R. In AG + ISO group, 30 minutes after aminoguanidine, 200 mg/kg i. p. isoflurane was inhaled as ISO group, and aminognanidine was injected 30 min before I/R in AG group. After 24 hours, the forebrains were collected, and the expression of Bcl-2 and Bax mRNA was determined by reverse transcriptase polymerase chain reaction. Results Bcl-2 mRNA expression in ISO group( 1.22 ±0. 12 ) was significantly higher than that in sham(0. 83 ±0. 16), I/R (0. 83 ±0. 11 )and AG + ISO group(0. 82 ±0. 12) ( P 〈 0.05 ). Bax mRNA expression in I/R and AG group was significantly higher than that in sham group ( P 〈 0.05 ), and the expression in ISO group was higher than that in AG + ISO group. Conclusion Nitric oxide is involved in the signaling pathway of isoflurane preconditioning and has the protection effect on gerbil brain against I/R.
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