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目的:探讨左旋咪唑加重大鼠实验性自身免疫性脑脊髓炎(EAE)是否通过上调抗原呈递细胞(APC)主要组织相容性复合体Ⅱ类抗原(MHC-Ⅱ)表达而实现的。方法:SD大鼠28只随机分为完全弗氏佐剂(CFA)组(n=8),EAE组(n=10),左旋咪唑组(n=10)。用豚鼠脊髓匀浆和CFA的混匀乳剂免疫SD大鼠制作EAE模型。在造模前3d至造模后7d腹腔注射左旋咪唑10mg·kg-1(左旋咪唑组)。分析各组行为学变化及神经组织病理学改变,用流式细胞术检测脾脏APC表面分子MHC-Ⅱ的表达。结果:左旋咪唑加速了大鼠EAE的病程,加重了神经缺损症状与中枢神经病理学损害;左旋咪唑上调了脾脏APC表面分子MHC-Ⅱ的表达,且与EAE神经缺损症状程度呈正相关。结论:左旋咪唑上调了APC表面分子MHC-Ⅱ的表达可能为左旋咪唑促发EAE的作用机制。
OBJECTIVE: To investigate whether levamisole increases the expression of major histocompatibility complex class Ⅱ antigen (MHC-Ⅱ) in experimental autoimmune encephalomyelitis (EAE) in rat antigen presenting cells (APC). Methods: Twenty - eight SD rats were randomly divided into complete Freund ’s adjuvant (CFA) group (n = 8), EAE group (n = 10) and levamisole group (n = 10). The EAE model was induced by immunizing SD rats with a mixed emulsion of guinea pig spinal cord homogenate and CFA. The rabbits were injected intraperitoneally with levamisole 10 mg · kg-1 (levamisole) 3d days before modeling to 7 days after modeling. The behavioral changes and neuropathological changes in each group were analyzed. The expression of MHC-II on the surface of APC was detected by flow cytometry. RESULTS: Levamisole accelerated the course of EAE in rats and aggravated the neurological deficits and central neuropathological damage. Levamisole up-regulated the expression of MHC-II on the surface of APC in spleen, and positively correlated with the severity of EAE. Conclusion: Levamisole up-regulates the expression of MHC-Ⅱ on APC surface and may be the mechanism of levamisole-induced EAE.