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作 者:陈晓莉[1] 陈毓茜[1] 王玉忠[1] 颜梅[1] 张俊美[1] 刘群[1] 杨欢[1] 李静[1]
出 处:《中南大学学报(医学版)》2012年第8期777-782,共6页Journal of Central South University :Medical Science
基 金:国家自然科学基金(30971033);湖南省科技计划基金(2008JT3016);中南大学研究生教育创新工程基金(2009ssxt167)~~
摘 要:目的:探讨miR-155在重症肌无力发病中的作用及地塞米松(dexamethasone,DXM)对miR-155的影响。方法:采用qPCR检测全身型重症肌无力(generalized myasthenia gravis,GMG)患者组和健康对照组B细胞,以及DXM干预后miR-155的相对表达量。用MTT法检测B细胞的增殖反应,流式细胞术检测DXM和PBS干预组B细胞表面CD80和CD86的表达,ELISA检测两组细胞上清液中抗AChR-IgG及其亚型IgG1,IgG2,IgG3的水平。结果:GMG外周血B细胞中miR-155的相对表达量高于健康对照组。DXM组B细胞中miR-155相对表达量低于PBS组;但两组之间B细胞的增殖及CD80和CD86的表达均无明显差异;DXM组培养上清中抗AChR-IgG1的水平低于PBS组,而抗AChR-IgG及其亚型IgG2,IgG3的水平无明显差异。结论:miR-155高表达可能参与重症肌无力的发病;糖皮质激素抑制miR-155的表达,可能通过调节B细胞的抗体类别转换发挥其治疗作用。Objective: To determine the role of miR-155 in the pathogenesis of generalized myasthenia gravis(GMG) and the effect of dexamethasone(DXM) on miR-155. Methods: The expression of miR-155 in B cells from the GMG patients and healthy controls was analyzed by qPCR.The B cells were cultured with DXM and PBS.The B cell proliferation was examined by MTT;CD80 and CD86 frequencies were detected by flow cytometry;and anti-AChR-IgG and isotypes anti-AChR-IgG1,2,3 in the supernatant were detected by ELISA. Results: qPCR revealed that the expression of miR-155 in the B cells was much higher than that in the controls,and the miR155 expression decreased after DXM treatment.flow cytometry showed that there was no significant difference in the proliferation and the expressions of CD80 and CD86 in the B cells between the DXM group and the PBS group.The concentration of anti-AChR-IgG1 was obviously lower in the DXM group than in the PBS group,but the concentration of anti-AChR-IgG,anti-AChR-IgG2,and anti-AchR-IgG3 was similar. Conclusion: high expression of miR-155 may be associated with myasthenia gravis progression.DXM may disturb the antibody class switch of B cells by suppressing the expression of miR-155 and improve the symptom of MG patients.
关 键 词:重症肌无力 MIR-155 地塞米松 抗体类别转换
分 类 号:R746.1[医药卫生—神经病学与精神病学]
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