黏附分子CD44介导的雌激素对实验性变态反应性脑脊髓炎大鼠保护作用的研究

Protective effect of estrogen mediated by the adhesion molecule CD44 on rats with experimental allergic encephalomyelitis

目的探讨雌激素对实验性变态反应性脑脊髓炎(EAE)大鼠的保护作用及其与黏附分子CD44的关系。方法将40只大鼠随机分为4个组:正常对照组、EAE组、大小剂量雌激素治疗组,每组10只。观察大鼠发病情况及脑组织病理变化,并采用免疫组织化学法检测各组大鼠脑组织CD44的含量。结果EAE组及大小剂量雌激素治疗组大鼠均有不同程度的发病,但大小剂量雌激素治疗组EAE临床症状均较EAE组轻。免疫组织化学显示,EAE组及大小剂量雌激素治疗组大鼠中枢神经系统(CNS)白质及灰白质交界处可见不同程度的CD44阳性细胞表达。图像分析结果显示,与EAE组比较,大小剂量雌激素治疗组CNS白质CD44表达水平均明显降低(P<0.01);与小剂量雌激素治疗组比较,大剂量雌激素治疗组CNS白质的CD44表达水平显著降低(P<0.01)。结论多发性硬化动物模型EAE大鼠中存在黏附分子CD44的高表达,雌激素可能通过抑制黏附分子CD44的表达而发挥对EAE大鼠的保护作用。

Objective To investigate the protective effect of estrogen on rats with experimental allergic encephalomyelitis(EAE)and its association with the adhesion molecule CD44.Methods A total of 40 rats were randomly divided into normal control group,EAE group,and highand lowdose estrogen treatment groups,with 10 rats in each group.The rats were observed in terms of disease onset and pathological changes of brain tissue,and immunohistochemistry was used to measure the content of CD44 in brain tissue.Results The rats in the EAE group and the highand lowdose estrogen treatment groups had disease onset with different severities,but the highand lowdose estrogen treatment groups had milder clinical symptoms than the EAE group.Immunohistochemistry showed varying degrees of the expression of CD44positive cells in the white matter and graywhite matter junction of the central nervous system(CNS)in the EAE group and the highand lowdose estrogen treatment groups.Image analysis showed that compared with the EAE group,the highand lowdose estrogen treatment groups had a significant reduction in the expression of CD44 in the CNS white matter(P<0.01),and compared with the lowdose estrogen treatment group,the highdose estrogen treatment group had a significant reduction in the expression of CD44 in the CNS white matter(P<0.01).Conclusions There is high expression of the adhesion molecule CD44 in the multiple sclerosis animal model of EAE,and estrogen may exert a protective effect on EAE rats by inhibiting the expression of the adhesion molecule CD44.