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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 observe the expression of CD200 in severe heat stroke rats and its relationship with the secretion of inflammatory cytokines and to explore the mechanism of CD200 involved in severe heat stroke. Methods Thirty - two male Wistar rats were randomly divided into control group (n = 8) and severe heat stroke group (HS, n = 24). The severe heat stroke group was placed in the artificial climate chamber at the temperature of (40 ± 2) ℃ and the humidity of (65 ± 5)%. The classic heat stroke model was prepared by thermal shock and the control group was placed at room temperature (22.0 ± 1) ℃. The rats were sacrificed at 0, 6, and 12 h after model establishment, respectively. Blood samples were collected for serum levels of high mobility group box 1 (HMGB1), tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) in lung tissue. The expression of CD200 mRNA was detected by RT-PCR. Results The expression of CD200mRNA in severe heat stroke group was lower than that in control group at each time point (P <0.05), and the expression of CD200mRNA gradually decreased after heat stroke (P <0.05). The levels of HMGB1, TNF-α and IL-6 were significantly higher than those of the control group (P <0.05). After heat shock, the secretion of HMGB1, TNF-α and IL-6 were gradually increased and increased in a time- The decrease of RNA expression was negatively correlated with the increase of HMGB1 (r = -0.635, P <0.05), TNF-α (r = -0.701, P <0.05) and IL-6 Sex. Conclusion Severe heat stroke, CD200 expression decreased and further reduced with time, the pro-inflammatory cytokines HMGB1, TNF-α and IL-6 secretion increased and gradually increased over time, CD200 expression decreased and HMGB1, TNF-α and IL-6 Increased secretion was negatively correlated. Aberrant expression of CD200 may be one of the molecular mechanisms of severe heatstroke inflammation.