白介素6在脂多糖致大鼠脑水肿中的表达

目的 探讨白介素6(IL-6)在脂多糖(LPS)致大鼠脑水肿发病过程中的表达及纳洛酮对其干预作用.方法 SD大鼠84只,对照组(NS组)28只,0.2ml生理盐水颈内动脉注射;内毒素组(LPS组)28只,颈内动脉注射LPS 200μg;纳洛酮治疗组(NAL组)28只,颈内动脉注射LPS后10min、1h、2h、6h、12h及处死前2h腹腔注射纳洛酮1mg/kg.于不同时间点测定脑组织匀浆IL-6的含量.干湿法测定脑组织含水量,甲酰胺法测定伊文思兰(EB)含量.结果 LPS组脑组织含水量和EB含量显著高于NS组(P＜0.01).NAL组脑组织含水量和EB含量显著低于LPS组(P＜0.01),但仍较NS组高(P＜0.01).注射LPS后4h,LPS组脑组织IL-6含量即增加,于6h达高峰,与NS组比较,差异有统计学意义(P＜0.01).NAL组IL-6含量低于LPS组(P＜0.05或P≤0.01),但高于NS组(P＜0.01).LPS组脑组织含水量和EB含量呈正相关(r=0.743,P＜0.01),IL-6含量与含水量呈正相关(r=0.459,P＜0.05),IL-6含量与EB含量呈正相关(r=0.568,P＜0.05).结论 IL-6参与脑水肿的发生发展,纳洛酮可以抑制IL-6的生成,减轻脑水肿.

Expression of interleukin 6 in brain edema induced by lipopolysaccharide in rats

Objective To study the expression of interleukin 6(IL-6) and the interfering effects of naloxone in the brain edema induced by lipopolysaccharide(LPS) in rats.Methods 84 SD rats were randomly devided into three groups:normal saline group(NS group,n=28),0.2ml normal saline was injected by carotid for each rat;LPS group(LPS group,n=28),the rat was applied 200ug LPS;Naloxone interfering group(NAL group,n=28),1mg/kg naloxone was intraperitoneally injected at 10min,1h,2h,6h,12h and 2h before decapitation following LPS injection.The content of IL-6 and even blue(EB) in brain tissue ware detected at different time points.The brain water content was measured by drying method.Results The content of water and EB in LPS group were significantly higher than that in NS group(P<0.01).In NAL group,the content of water and EB were significantly lower than that in LPS group(P<0.01),but higher than that in NS group(P<0.01).In LPS group,IL-6 content was significantly higher than NS group(P<0.01).At 4h,6h and 12h,IL-6 content was significantly higher than NAL group(P<0.05or P<0.01),but at 24h,no significant difference was seen in two groups.In LPS group,water content and EB content were positively correlated(r=0.743,P<0.01);IL-6 content and water content had positive relationship(r=0.459,P<0.05).IL-6 content and EB content had positive relationship(r=0.568,P<0.05).Conclusion IL-6 could participate in the onset and development of brain edema induced by LPS.NAL has therapeutic effect by affecting the production of IL-6.