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目的:观察CD200预处理对重症中暑大鼠炎症反应的影响,探讨CD200参与重症中暑炎症反应的机制。方法:将40只雄性Wistar大鼠随机分为对照组(n=8)、重症中暑模型组(HS组,n=16)、CD200预处理组(CD200组,n=16)。HS组和CD200预处理组在热暴露前分别尾静脉注射生理盐水和CD200重组融合蛋白,制备经典中暑模型,对照组置于(22.0±1)℃室温下。分别于造模后60min时点检测肺组织CD200mRNA表达,检测血清高迁移率族蛋白B1(HMGB1)、肿瘤坏死因子α(TNF-α)和白介素6(IL-6)浓度。记录大鼠重症中暑形成时间、生存时间。结果:HS组和CD200预处理组CD200 mRNA表达均低于对照组(P<0.05);HS组和CD200预处理组血清中HMGB1、TNF-α、IL-6均明显高于对照组(P<0.05),HS组HMGB1、TNF-α、IL-6高于CD200预处理组(P<0.05);CD200预处理组相比HS组在重症中暑形成时间(P<0.05)和中位生存时间(P<0.05)均延长。结论:CD200的表达异常可能是重症中暑炎症反应的分子机制之一,CD200预处理可以减轻重症中暑大鼠炎症反应,改善热应激状态下大鼠的预后。
OBJECTIVE: To observe the effect of CD200 pretreatment on the inflammatory response in severe heat stroke rats and to explore the mechanism of CD200 involved in severe heat stroke. Methods: Forty male Wistar rats were randomly divided into control group (n = 8), severe heat stroke model group (HS group, n = 16) and CD200 pretreatment group (n = 16). HS group and CD200 pretreatment group were injected normal saline and CD200 recombinant fusion protein respectively before heat exposure to prepare classic heat stroke model and the control group was placed at room temperature (22.0 ± 1) ℃. The expression of CD200 mRNA in lung tissue was detected at 60 min after model establishment. The serum levels of HMGB1, TNF-α and IL-6 were measured. The incidence of severe heat stroke in rats was recorded and the survival time was recorded. Results: The expressions of CD200 mRNA in HS group and CD200 pretreatment group were lower than those in control group (P <0.05). The serum levels of HMGB1, TNF-α and IL-6 in HS group and CD200 pretreatment group were significantly higher than those in control group (P < 0.05). The levels of HMGB1, TNF-α and IL-6 in HS group were higher than those in CD200 pretreatment group (P <0.05) P <0.05) were extended. Conclusion: The abnormal expression of CD200 may be one of the molecular mechanisms of severe heat stroke. CD200 pretreatment can reduce the inflammatory response in severe heatstroke rats and improve the prognosis of rats under heat stress.