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利多卡因对脑缺血再灌注损伤大鼠海马组织细胞间黏附分子-1及核转录因子-κB表达的影响
Effects of lidocaine on the expression of intercellulor adhesion molecule-1 and NF-κB in hippocampus following cerebral ischemia-reperfusion in rats
【摘要】 目的观察利多卡因对大鼠脑缺血再灌注损伤后海马组织细胞间黏附分子-1(ICAM-1)及核转录因子-κB(NF-κB)蛋白和mRNA表达的影响,探讨利多卡因脑保护作用的机制。方法雄性SD大鼠32只,随机分为假手术组(A组)、缺血再灌注组(B组)、利多卡因小剂量组(C组)和利多卡因大剂量组(D组),缺血前10 min腹腔注射。脑缺血10 min再灌注24 h时,断头处死大鼠。用RT-PCR技术检测海马组织ICAM-1及NF-κB mRNA的表达,用免疫组织化学、蛋白印记(Western blot)方法检测ICAM-1及NF-κB蛋白表达情况。结果脑缺血再灌注后海马组织ICAM-1和NF-κB mRNA及蛋白表达水平增高,利多卡因可下调ICAM-1及NF-κB表达;缺血再灌注后,海马区神经元出现明显坏死,利多卡因可减轻海马区神经元损伤。结论利多卡因可能通过抑制ICAM-1与NF-κB基因表达而对脑缺血再灌注损伤起到一定的保护作用。
【Abstract】 Objective To investigate the effects of lidocaine on the expression of intercellulor adhesion molecule-1 and nuclear transcription factor-kappa B(NF-κB) protein and mRNA in hippocampus following global cerebral ischemia-reperfusion(I/R)in rats.Methods A total of 32 male SD rats weighing 250-300g were randomly divided into 4 groups: group A sham-operated(n=8);group B I/R(n=8) and group C I/R+5mg lidocaine;group D(I/R)+10mg lidocaine.Cerebral I/R was produced by Longa’s method.Reperfusion was done after 10min of cerebral ischemia.The animals were decapitated at the end of 24h reperfusion and the brains were removed.The levels of ICAM-1 and NF-κB mRNA,protein expression in the hippocampus were detected by RT-PCR,Western bloting and immunohistochemistry,respectively.Results I/R induced ICAM-1 and NF-κB mRNA and protein expression in the hippocampus.Intraperitoneal lidocaine pretreatment significantly inhibited the ICAM-1 and NF-κB expression in hippocampus(B vs.C,D,P<0.01).Conclusion Cerebral I/R induces significant increase in the expression of ICAM-1 and NF-κB,and lidocaine pretreatment can significantly inhibit I/R induced ICAM-1 and NF-κB expression.
【Key words】 docaine; intercellulor adhesion molecule-1; nuclear transcription factor-kappa B; cerebral ischemia-reperfusion; hippocampus; rat;
- 【文献出处】 西安交通大学学报(医学版) ,Journal of Xi’an Jiaotong University(Medical Sciences) , 编辑部邮箱 ,2006年06期
- 【分类号】R743.3
- 【被引频次】8
- 【下载频次】184