CD200调节重症中暑大鼠肺部炎症反应的信号通路初探  

A preliminary study of signal pathway to alleviate pulmonary inflammation response by CD200 in rats with severe heatstroke

作　　者：陈荣琳[1] 曹枫[1] 符少平[1] 彭怀力[1] 施学智 梁泳欣 童华生 Chen Rong-Lin;Cao Feng;Fu Shao-Ping;Peng Huai-Li;Shi Xue-Zhi;Liang Yong-Xin;Tong Hua-Sheng(Department of Intensive Care Medicine,Longgang Central Hospital,Shenzhen 518116,China;Department of Intensive Care Medicine,Southern Theater General Hospital of PLA,Key Laboratory of Trauma and Tissue Repair of Tropical Area of PLA,Guangzhou 510010,China)

机构地区：[1]深圳市龙岗中心医院重症医学科,深圳518116 [2]解放军南部战区总医院重症医学科/解放军热区损伤与组织修复重点实验室,广州5100010

出　　处：《解放军医学杂志》2020年第3期265-269,共5页Medical Journal of Chinese People's Liberation Army

基　　金：军事医学创新工程专项(18CXZ032);广东省科技计划项目(2017A020215055);广东省深圳市龙岗区科技创新局资助项目(LGKCYLWS2018000034)。

摘　　要：目的观察CD200预处理对重症中暑大鼠炎性因子和肺组织NF-κB表达的影响,探索NF-κB在CD200抑制重症中暑大鼠肺部炎症反应中的作用。方法雄性Wistar大鼠40只,随机分为对照组(n=8)、重症中暑组(HS组,n=16)、CD200预处理组(CD200组,n=16)。HS组、CD200组分别注射等体积生理盐水和CD200融合蛋白,然后经热打击制备大鼠重症中暑模型;对照组饲养于(22.0±1.0)℃环境。造模后60 min检测大鼠肺组织NF-κB/p65 mRNA表达,测定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)水平,观察肺组织病理形态学改变,记录大鼠存活时间。结果 HS组和CD200组大鼠肺组织NF-κB/p65 mRNA表达水平明显高于对照组(P<0.05),且HS组高于CD200组(P<0.05)。HS组、CD200组和对照组血清HMGB1水平分别为(42.63±18.51、34.12±10.01、5.27±2.31) pg/ml,TNF-α水平分别为(138.58±50.89、63.54±25.25、19.32±8.82) ng/ml,IL-6水平分别为(115.65±40.15、51.08±15.08、7.25±2.28) ng/ml,HS组和CD200组均显著高于对照组(P<0.05),且HS组高于CD200组(P<0.05)。CD200组大鼠存活时间明显长于HS组[(98.4±21.6) min vs.(81.4±18.3) min,P<0.05]。病理形态学观察显示CD200组炎症及肺泡渗出相较HS组明显减轻。结论 CD200预处理可以减轻重症中暑大鼠的炎症反应,这一作用可能涉及NF-κB的活化抑制及炎性因子表达降低。Objective To observe the changes of NF-κB and inflammatory cytokine expression after CD200 pretreatment in severe heatstroke rats for exploring whether the molecular mechanism of CD200 inhibition of severe heat stroke inflammatory response is related to NF-κB signaling pathway. Methods Forty male Wistar rats were randomly divided into control group(n=8), severe heatstroke model group(HS group, n=16), and CD200 pretreatment group(CD200 group, n=16). The HS group and the CD200 group were injected with physiological saline and CD200 recombinant fusion protein before heat exposure to prepare a classical rat heat stroke model, and the control group was placed at room temperature of 22.0±1.0 ℃. The expression of NF-κB/p65 mRNA in lung tissue were detected at 60 min after model establishment, and serum high mobility group protein B1(HMGB1), tumor necrosis factor alpha(TNF-α) and interleukin 6(IL-6) were detected. The pathological changes of the lungs were observed, and the survival time of severe heatstroke rats were recorded. Results CD200 pretreatment could inhibit the expression of NF-κB/p65 mRNA. Compared with the control group, the expressions of NF-κB/p65 mRNA in the HS group and CD200 group were significantly increased(P<0.05), and the expression of NF-κB/p65 mRNA in CD200 group was lower than that in HS group(P<0.05). Serum HMGB1, TNF-α and IL-6 in HS group and CD200 group were significantly higher than those in the control group(P<0.05). The HMGB1, TNF-α and IL-6 in the HS group were higher than those in the CD200 group(P<0.05). The median survival time of severe heat stroke were prolonged in the CD200 group compared with the HS group(P<0.05), and the pathomorphological changes showed that inflammation and alveolar exudation were significantly reduced in the CD200 group compared with the HS group. Conclusions CD200 pretreatment can alleviate the inflammatory response in severe heatstroke rats. The possible molecular mechanism of CD200 to relieve severe heatstroke inflammatory response may be involve

关 键 词：重症中暑 CD200 NF-ΚB 炎症反应 细胞因子 

分 类 号：R594.12[医药卫生—内科学]