摘要
目的 探讨血浆 β 内啡肽 ( β endorphin ,β EP)在创伤失血性休克后以脾细胞IL 2R表达及IL 2分泌为代表的细胞免疫调节中的作用。方法 ①采用大鼠创伤失血性休克模型 ,收集休克前、休克后 0、1、3、6、12、2 4h休克血浆 (SP) ,并检测SP中 β EP水平 ;②采用体外实验 ,分离并混合 4只正常大鼠脾细胞 ,分别与SP、SP +β EP抗血清体外培养 ,观察conA诱导的脾细胞IL 2分泌及IL 2R表达的变化。结果 ①休克后即刻血浆 β EP水平显著升高 (P <0 .0 1) ,1h达高峰 ,之后呈下降趋势 ,2 4h趋于休克前水平。②与对照组相比 ,SP可显著降低conA诱导的脾细胞功能 (P <0 .0 1) ,SP中 β EP含量与脾细胞IL 2分泌及IL 2R表达呈显著负相关 (P <0 .0 1) ;SP经 β EP抗血清处理组较未处理组相比 ,脾细胞功能明显升高 (P <0 .0 5 ) ,但仍低于对照组。结论 创伤失血性休克后血浆中显著升高的 β
Objective To investigate the role of plasma β endorphin(β EP) in the regulation of cellular immunity, mainly IL 2R expression and IL 2 production in rat splenic cells, following traumatic hemorrhagic shock(T HS). Methods ①Wistar rats with T HS were used and sacrificed at 0, 1, 3, 6, 12 and 24 h after T HS. Plasma specimens were collected and β EP levels in plasma were detected. Rats with sham operation were served as the controls. ②Models of in vitro experiment were used. Spenic cells were isolated and mixed from four normal rats and cocultured with shock plasma or shock plasma+β EP antiserum. ConA induced splenic cell IL 2 production and IL 2R expression were observed. Results ①Level of plasma β EP increased remarkably after T HS immediately, peaked at 1 h, showed decreasing tendency and restored to pre shock level 24 h after T HS. ②Shock plasma significantly suppressed ConA induced splenic cell function; Levels of plasma β EP were negatively correlated with IL 2 production and IL 2R expression in spenic cells; Compared with that in SP group, splenic cell function elevated markedly in SP+β EP antiserum group, but was still lower than that in controls. Conclusion The increased plasma β EP following T HS is involved in the suppression of cellular immunity.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2003年第8期657-659,共3页
Journal of Third Military Medical University
基金
全军"九五"指令性课题 ( 96L0 4 1)
