中枢神经系统感染与脑血管内皮细胞表面E选择素的表达

Expression of E-selectin in cerebrovascular endothelium in a brain inflammation model

目的 研究中枢神经系统感染时血管内皮细胞E选择素的表达 ,以及地塞米松对其抑制作用。方法 将 5 4只小鼠随机分成侧脑室注射内毒素 (2 0 μg/2 0 μl)组、腹腔注射地塞米松 [1mg/(kg·12h) ]+侧脑室注射内毒素 (2 0 μg/2 0 μl)组、生理盐水组以及空白对照组。免疫组织化学法观察脑血管内皮细胞E选择素的表达 ,HE染色观察脑组织炎症反应。结果 空白对照组有少量E选择素表达 [(13 7± 2 7) %]。生理盐水组 [(13 5± 5 6 ) %]与空白对照组E选择素表达比较差异无显著性。内毒素组注射后E选择素表达在第 1天 [(31 8± 10 5 ) %]、第 2天 [(2 6 8± 9 6 ) %]明显增多 ,与生理盐水组比较差异有显著性 (P <0 0 1或 <0 0 5 ) ,注射后第 3天 [(15 7± 9 9) %]恢复正常 (P >0 0 5 ) ;注射后 3d内E选择素表达呈进行性下降 (F =4 0 8,P <0 0 5 )。地塞米松 +内毒素组于注射后第 1天和第 2天E选择素表达与内毒素组比较明显受到抑制 ,分别为 (13 0± 12 4 ) %、(8 8±6 0 ) %(P略 >0 0 5 ,P <0 0 5 ) ,与生理盐水组比较差异无显著性 ;同时脑组织炎症反应受到明显抑制。结论 中枢神经系统感染时脑血管内皮细胞E选择素的表达增加 ;地塞米松可通过抑制脑血管内皮细胞表面E选择素的表达来抑制炎症反应?

Objective This study was aimed to explore the changes of expression of E-selectin on the cerebrovascular endothelium in the central nervous system with the inflammation and to evaluate the roles of dexamethasone. Methods Fifty-four mice were randomly divided into the following groups: endotoxin (20 μg/20 μl of saline) group, endotoxin (20 μg/20 μl of saline) plus dexamethasone [i.p.,1 mg/(kg·12h)] group, saline group and controls. The information of E-selectin expression in the cerebrovascular endothelium was obtained by observing brain tissue sections staining with the immunohistochemical method. HE staining on brain tissue sections was also performed to observe the profile of the brain inflammation reaction induced by endotoxin. Results A weak expression of E-selectin was found in the control group [(13.7±2.7)%]. The administration of saline [(13.5±5.6)%] did not affect E-selectin expression. As compared to the saline group, E-selectin expression in the endotoxin group was significantly enhanced at day 1 [(31.8±10.5)%, t = 3.77, P<0.01] and day 2 [(26.8±9.6)%, t=2.94, P<0.05] with the inflammation reactions including the brain edema, intravascular adhesion, extravascular infiltration of lymphocytes and neutrocytes, and enlarged surrounding interstitium of vascules. After 3 days of the endotoxin injection, the E-selcetin expression [(15.7±9.9)%, t=0.47, P>0.05] was similar to that of the saline group, and the inflammation reaction was mildened. The E-selectin expression was progressively declined during the first 3 days of the injection (F=4.08,P<0.05). As compared to the endotoxin group, the E-selectin expression in the endotoxin plus dexamethasone group was significantly inhibited at day 1 [(13.0±12.4)%, t=2.16, P<0.05] and day 2 [(8.8±6.0)%, t=2.64, P<0.05], and the inflammation reactions were significantly blocked by the injection of dexamethasone. No differences in the expression of E-selectin were found among the endotoxin plus dexamethasone group (at day 1, 2 and 3) , the saline group and controls (all P>0.05). Conclusion The over-expression of E-selectin on vessel endothelial cells of brain may be involved in the process of inflammation of the central nervous system. Dexamethasone may inhibit the brain inflammatory reaction, possibly through its inhibition of the E-selectin expression on vessel endothelial cells.