摘要
目的观察CD200在重症中暑大鼠中的表达与变化规律,及其与炎症因子分泌的关系,初步探讨CD200参与重症中暑炎症反应的机制。方法将雄性Wistar大鼠32只,随机分为对照组(n=8)、重症中暑组(HS,n=24)。重症中暑组置于人工气候舱内,温度(40±2)℃,湿度(65±5)%,热打击制备经典中暑模型,对照组置于(22.0±1)℃室温下。分别于造模后0、6、12 h时点采血并处死大鼠,抽血用酶联免疫法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,采用RT-PCR法检测肺组织CD200 m RNA表达。结果重症中暑组各时点CD200m RNA表达均低于对照组(P<0.05),热打击后CD200 m RNA表达逐渐降低,且呈时间依赖性递减(P<0.05);重症中暑组血清中HMGB1、TNF-α、IL-6均明显高于对照组(P<0.05);热打击后HMGB1、TNF-α、IL-6分泌逐渐上调,且呈时间依赖性升高(P<0.05);CD200 m RNA表达降低与HMGB1(r=-0.635,P<0.05),TNF-α(r=-0.701,P<0.05),IL-6(r=-0.786,P<0.05)浓度升高呈显著负相关性。结论重症中暑时,CD200表达减少并随着时间进一步降低,促炎细胞因子HMGB1、TNF-α和IL-6分泌增多并随时间逐渐升高,CD200表达减少与HMGB1、TNF-α和IL-6分泌增多呈负相关。CD200的表达异常可能是重症中暑炎症反应的分子机制之一。
Objective To investigate the relationship and mechanism between the expression of CD200 and the serum levels of inflammation mediators in rats with severe heatstroke(HS). Methods Thirty-two male Wistar rats were randomly divided into a normal control group(n=8)and a heatstroke group(HS group,n=24). The rats of the HS group were placed in an artificial climate chamber [temperature(40±2)℃,humidity(65±5)%] to induce HS,while the rats of the control group were kept at room temperature(22±1)℃. The HS group rats were sacrificed in batches at 0,6 and 12 h after successful modeling. The levels of high mobility group protein B1(HMGB1),tumor necrosis factor α(TNF-α),and interleukin-6(IL-6)were determined. The expression of CD200 mRNA was also assayed by RT-PCR. Results The expression of CD200 mRNA was significantly decreased after the heat treatment(P〈0.05),and it showed a gradual decrement trend performance over time(P〈0.05). Compared with the control group,HMGB1,IL-6,and TNF-α were increased after the heat treatment(P〈0.05),and this effect was enhanced with the prolongation of exposure time(P〈0.05). There was a negative correlation between the expression of CD200 mRNA and the serum levels of HMGB1(r =-0.635,P〈0.05),TNF-α(r =-0.701,P〈0.05),and IL-6(r =-0.786,P〈0.05). Conclusion The expression rate of CD200 decreases significantly in rats with severe heatstroke,in the meantime,the serum levels of HMGB1,TNF-α,and IL-6 increase significantly. There is a negative correlation between the CD200 decrease and HMGB1,TNF-α,and IL-6 increases. These results indicate that CD200 might participate in the pathogenesis of inflammation in severe heatstroke.
出处
《中国热带医学》
CAS
2016年第8期762-765,共4页
China Tropical Medicine
基金
国家自然科学基金(No.81471839)
深圳市科创委知识创新计划资助项目(No.JCYJ20150403091931177)