交感神经活性对大脑中动脉闭塞大鼠外周免疫功能的影响  

Effect of sympathetic activity on peripheral immune function of middle cerebral artery occlusion in rats

作　　者：张金华[1,2] 闫福岭[1] 

机构地区：[1]东南大学附属中大医院神经内科,南京210009 [2]南京同仁医院神经内科,211100

出　　处：《国际脑血管病杂志》2011年第2期111-114,共4页International Journal of Cerebrovascular Diseases

基　　金：江苏省自然科学基金（BK2008299）;卫生部科研基金（LW201007）

摘　　要：目的探讨交感神经系统活性变化与脑梗死后外周细胞免疫功能抑制之间的关系。方法成年雄性Sprague-Dawley大鼠制作大脑中动脉闭塞（middle cerebral artery occlusion，MCAO）模型。采用双抗体夹心酶联免疫吸附法测定大鼠血清促炎细胞因子白细胞介素（interleukin，IL）-1β、干扰素-γ（interferon-γ，IFN-γ）和抗炎细胞因子IL-10水平，以评价外周细胞免疫状态；采用竞争性酶联免疫吸附法测定大鼠血清3一甲基肾上腺素（metanephfine，MN）和去甲-3-0-甲基肾上腺素（nonneta-nephrine，NMN）水平。腹腔注射β-受体阻滞药普萘洛尔阻断交感神经活性后，检测交感神经活性和促炎航炎细胞因子水平。结果与假手术组相比，脑梗死组大鼠血清MN和NMN水平在MCAO后6h开始升高，72h达高峰，然后缓慢下降，MCAO后2周时仍显著高于假手术组（P〈0．01）。在MCAO后72h，普萘洛尔干预组的MN和NMN水平显著降低（P〈0．01），促炎细胞因子IL-1β和IFN-γ水平显著升高（P〈0．01），抗炎细胞因子IL-10水平显著降低（P〈0．01）。结论脑梗死大鼠交感神经过度激活，外周细胞免疫处于抑制状态；阻断交感神经功能后外周免疫抑制基本逆转，提示交感神经过度激活在脑梗死后的免疫抑制过程中可能起重要作用。Objective To investigate the relationship between the changes of the sympathetic nervous system activity and the peripheral cellular immunodepression after cerebral infarction. Methods An adult male Sprague-Dawley rat model of middle cerebral artery occlusion （MCA0） was induced. A double-antibody sandwich enzyme-linked immunosorbent assay was used to detect the levels of serum proinflammatory cytokines interleukin （IL） -1β, interferon-γ （TNF-γ） and anti-inflammatory cytokines IL-10. A competitive enzyme-linked immtmosorbent assay was used to detect the levels of serum metanephrine （MN） and normetanephrine （NMN）. After blocking sympathetic activity by injecting 13 -blocker propranolol intraperitoneally, the sympathetic activity and the levels of pro/anti-inflammatory cytokines were detected. Results The levels of serum MN and NMN at 6 hours after MCAO began to increase in the cerebral infarction group compared with the sham operation group. They reached the peak at 72 hours, and then decreased slowly. However, they were still higher than those in the sham operation group 2 weeks after MCAO （P 〈 0. 01 ）. At 72 hours after MCAO, the levels of MN and NMN in the propranolol intervention group were decreased significantly （P 〈0. 01）, the levels of proinflammatory cytokines IL-1 [3 and INF-＇vwere increased significantly （P 〈0. 01）, and the levels of anti-inflammatory cytokine IL-10 were decreased significantly （P 〈0. 01）. Conclusions When sympathetic nervous system is overactivated after cerebral infarction in rats, the peripheral cellular immunity is in a state of depression; the peripheral immunodepression will be fundamen- tally reversed after blocking the sympathetic function, and this suests that the overactivation of sympathetic nervous system may play a important role in the process of immunodepression after cerebral infarction.

关 键 词：交感神经系统 免疫系统 脑缺血 细胞因子 疾病模型 动物 大鼠 

分 类 号：R74[医药卫生—神经病学与精神病学]