阻断糖皮质激素受体的抗骨折伤免疫抑制作用

复制大鼠股骨骨折模型,用RU486(10mg/kg)阻断模型大鼠的糖皮质激素受体(GR)。发现致伤早期阻断GR可有效地阻止骨折伤诱导的免疫抑制,使淋巴细胞的增殖活性、血浆IgG、IgM、C3水平和脾/体重比高于空白对照组(P<0.01)。连续3d阻断GR的抗骨折伤免疫抑制的作用减弱,上述指标高于空白对照组(P<0.05),但低于早期GR阻断组。结果提示,GR介导信号对创伤早期的免疫反应起重要作用,适当切断其功能有利于保护创伤大鼠的免疫功能。

EFFECTS OF BLOCKING GLUCOCORTICOID RECEPTOR ON BONE FRACTURE INDUCED IMMUNOSUPPRESSION IN RATS

The effects of blocking glucocorticoid receptor (GR) on bone fracture induced immunosuppression in rats were studied. The immune responses of cells T and B to Con A, concentrations of IgG, IgM and C3 in these animals' sera and the rate of their spleen weight to body weight decreased (P<0. 01) after bone fracture in for 96 h, compared with those of the control rats. The immunosuppression could be prevented partially by blocking GR with 10mg/kg of RU486 in 1 and 24h when bone was fractured later. Then all of the immune indexes in these groups were higher than that of the control (P<0. 01). If GR was blocked continuously for 3 days with RU486, the immunosuppression also could be prevented partially. but was lower than that of group blocking GR in early period. The results indicate that GR plays an important role in trauma - induced early immunosuppression and the immunosuppression can be prevented partially by blocking GR.