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目的探讨热射病小鼠早期(0~24 h)中枢神经炎症和外周炎症的变化及其相关性。方法 70只BALB/c雄性小鼠按随机数字表法分为正常对照组和热射病后各时相(0、1、6、12、24 h)观察组。应用环境模拟舱建立热射病小鼠模型。观察记录各组小鼠生存率、直肠温度变化和体质量变化,Real-time PCR检测大脑皮层和海马炎症因子TNF-α、IL-1β和IL-6的表达,ELISA测定外周血清中炎症因子TNF-α、IL-1β和IL-6的分泌情况,鲎试剂动态浊度法检测血清中内毒素浓度。结果热暴露后小鼠直肠温度超过42℃,1~2 h出现低温期,24 h后小鼠存活率为78.57%,成功制备热射病小鼠模型;大脑皮层及海马在热暴露后1 h炎症因子TNF-α、IL-1β、IL-6的基因表达显著增加并达到最高峰值(P<0.01),6 h后逐渐降低但仍明显高于正常对照组(P<0.01),24 h后基本恢复至正常对照组水平(P>0.05);外周血清中炎症因子TNF-α、IL-1β和IL-6在1 h后含量显著增加(P<0.01),之后缓慢下降,到24 h后仍高于正常对照组(P<0.01);血清内毒素在热暴露即刻(0 h)开始明显升高,6 h后达到峰值,至24 h仍明显高于正常对照组(P<0.01)。结论热射病小鼠在热暴露12 h内中枢神经系统出现一过性炎症反应,而外周炎症反应持续至24 h之后,提示热射病小鼠早期中枢神经炎症反应与外周炎症反应可能是相互独立发生。
Objective To investigate the changes and correlations of central nervous system inflammation and peripheral inflammation in early-stage (0-24 h) pyrexia mice. Methods Seventy BALB / c male mice were randomly divided into normal control group and observation group (0, 1, 6, 12, 24 h) after heat stroke. Establishment of a mouse model of heat-induced fever using environmental simulator. The changes of survival and rectal temperature and body weight of mice in each group were observed and recorded. The expression of TNF-α, IL-1β and IL-6 in cerebral cortex and hippocampus were detected by Real-time PCR. The levels of inflammatory cytokines TNF -α, IL-1β and IL-6 secretion, 鲎 reagent dynamic nephelometry detection of serum endotoxin concentration. Results After rectal exposure to heat, the rectal temperature of the mice was over 42 ℃, the hypothermia was observed within 1-2 h, and the survival rate of mice was 78.57% after 24 h. The mouse model of heat-induced arthritis was successfully established. The cerebral cortex and hippocampus were exposed 1 h The gene expression of inflammatory factors TNF-α, IL-1β and IL-6 increased significantly (P <0.01) and gradually decreased after 6 h, but still significantly higher than that of normal control group (P <0.01) (P> 0.05). The levels of inflammatory cytokines TNF-α, IL-1β and IL-6 in peripheral serum were significantly increased after 1 h (P <0.01), and then decreased slowly. (P <0.01). The level of endotoxin in serum increased significantly immediately after heat exposure (0 h), peaked at 6 h, and remained significantly higher at 24 h than that of the normal control group (P <0.01). Conclusions There is a transient inflammatory reaction in the central nervous system within 12 h after heat exposure in the mice with thermal radiation, while the peripheral inflammatory reaction lasts up to 24 h, suggesting that the early central nervous system inflammatory reaction and the peripheral inflammatory reaction may be mutual Happen independently