实验性自身免疫性脑脊髓炎大鼠脑组织PGE_2表达的研究

目的检测实验性自身免疫性脑脊髓炎(EAE)大鼠脑组织PGE2表达情况,探讨其在EAE发病过程中的作用。方法将30只Wistar雌性大鼠随机分为正常对照组、佐剂对照组及EAE模型组,各10只,使用新鲜豚鼠脊髓匀浆(GPSCH)与含卡介苗(BCG)的弗氏完全佐剂(CFA)建立EAE模型。对各组大鼠发病潜伏期、进展期及发病高峰期神经功能障碍评分进行记录,采用免疫组织化学方法检测大鼠脑组织前列腺素E2(PGE2)的表达,并用Image Pro Plus软件对PGE2含量进行平均光密度值测定。结果正常对照组及佐剂对照组大鼠未发病,EAE模型组大鼠均发病。正常对照组及佐剂对照组大鼠脑组织中未见PGE2表达,EAE模型组大鼠脑组织中则可见PGE2表达,且PGE2含量与EAE大鼠发病潜伏期呈负相关,与发病进展期及发病高峰期神经功能障碍评分呈正相关。结论 PGE2可能参与了EAE疾病的发生发展过程。

Objective To detect the expression of prostaglandin E 2 （PGE 2） in＇the brain tissue of experimental autoimmune encephalomyelitis （EAE） and investigate the effect of PGE 2 on EAE. Methods Thirty female Wistar rats were randomly divided into three groups according to the randomly digital table： normal control group, EAE control group and adjuvant group. The complexes of the guinea pig spinal cord homogenate （GPSCH） and the complete FrReud＇ s adjuvant （CFA） were used in the induction of the Wistar rat model of EAE. The latency, progression and scores of symptoms were recorded. The expressions of PGE2 in the brain tissue were detected by the immunohistochemistry technique and the staining intensities of PGE 2 were semiquantitatively analysised with the ImagePro Plus. Results No rats in the normal control and adjuvant group were ill while rats in the EAE control group were just opposite. Compared with the normal control and adjuvant group, there were significantly obvious expressions of PGE2 in EAE control. The expressions of PGE 2 were negatively correlated with the latencies of this disease while positively correlated with the progressions and the scores of symptoms in the peak time of this disease. Conclusion PGE 2 might play a role in the development of EAE.