δ、κ、μ受体在创伤失血性休克大鼠细胞免疫抑制中的作用  

Role of opioid receptors δ, κ and μ in suppression of cellular immunity following traumatic hemorrhagic shock in rats

作　　者：文爱清[1] 王军[2] 刘良明[1] 胡德耀[1] 

机构地区：[1]第三军医大学附属大坪医院野战外科研究所第二研究室,重庆400042 [2]第三军医大学附属大坪医院消化科,重庆400042

出　　处：《中华创伤杂志》2002年第11期692-695,共4页Chinese Journal of Trauma

基　　金：全军"九五"指令性课题基金资助项目 ( 96L0 41)

摘　　要：目的　探讨何种阿片受体亚型介导了血浆β -内啡肽 ( β -endorphin ,β -EP)在创伤失血性休克后免疫抑制中的作用。　方法　采用体外实验 ,分别以δ、κ、μ受体高选择性拮抗剂nal trindole(NTI)、nor-binaltorphimine(Nor-BNI)和小剂量纳洛酮 (naloxone ,NAL ,相对选择性 μ受体拮抗剂 )为工具药 ,作用于休克 1h血浆处理的脾细胞 ,观察刀豆素A诱导的脾细胞增殖、白细胞介素 -2 (IL - 2 )分泌及白细胞介素 - 2受体 (IL - 2R)表达的变化。实验分休克血浆组 (Ⅰ组 )、受体拮抗剂治疗组 (Ⅱ组 )、受体拮抗剂自身对照组 (Ⅲ组 )及基础对照组 (Ⅳ组 )。　结果　Ⅱ组与Ⅰ组相比 ,10 μmol/LNAL(非选择性阿片受体拮抗剂 )非常显著地增强脾细胞增殖功能、IL - 2分泌和IL - 2R表达 (P <0 .0 1) ;小剂量NAL( 1～ 10 0nmol/L)对各项观察指标均无明显影响。NTI和Nor-BNI显著降低休克血浆对脾细胞增殖功能、IL - 2的分泌及IL - 2R表达的抑制 (P <0 .0 5或P <0 .0 1) ;但各项指标都仍然未恢复到正常水平 (P <0 .0 1)。Ⅲ组与Ⅳ组相比 ,NTI抑制脾细胞增殖功能、IL - 2的分泌和IL - 2R的表达 ,其中 10 0 0nmol/L的NTI抑制效果较显著 (P <0 .0 5 )。Nor -BNI和NAL自身对照组对各指标均无显著影响。　结论　创伤失血性休?Objective To explore subtypes of opioid receptors involving in the suppression of cellular immunity following traumatic hemorrhagic shock (THS). Methods All the experiments were done in vitro. Selective antagonists such as naltrindole (NTI), nor-binaltorphimine (Nor-BNI) and naloxone (NAL) of the receptors δ, κ and μ were used as tool drugs and added to the normal splenic cell culture treated with shock plasma so as to observe the parameters like ConA-induced splenic cell proliferation, IL-2 production and IL-2R expression. The rats were divided into shock plasma group (Group Ⅰ), receptor antagonist treatment group (Group II), receptor antagonist self-control group (Group III) and baseline group (Group Ⅳ). Results Compared with the Group I, 10 μmol/L of NAL significantly elevated ConA-induced splenic cell proliferation, IL-2 production and IL-2R expression in the Group Ⅱ. While small doze of NAL (1-100 nmol/L) had no effect. NTI and Nor-BNI obviously decreased suppression on splenic cell proliferation, IL-2 production and IL-2R expression by shock plasma (P<0.05 or P<0.01). However, all the parameters did not recover to normal level (P<0.05). In the Group III, NTI suppressed splenic cell proliferation, IL-2 production and IL-2R expression and reached a significant level at doze of 1 000 nmol/L (P<0.05), compared with the Group Ⅳ. On the contrary, Nor-BNI and NAL had no significant effect on all parameters. Conclusions After THS, peripheral β-endorphin mediated immunosuppressive effect mainly by means of receptors δ and κ without correlation with receptor μ.

关 键 词：受体 创伤 失血性休克 大鼠 Β-内啡肽 免疫抑制 

分 类 号：R392[医药卫生—免疫学]