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机构地区:[1]广西医科大学第一附属医院心内科,广西心血管病研究所,广西南宁530021
出 处:《细胞与分子免疫学杂志》2014年第6期601-603,607,共4页Chinese Journal of Cellular and Molecular Immunology
基 金:国家自然科学基金(81160032)
摘 要:目的观察IL-17A对病毒性心肌炎(VMC)小鼠血清抗心肌抗体水平的影响。方法雄性野生型(WT)和IL-17A基因敲除型(IL-17A-/-)BALB/c小鼠,腹腔注射柯萨奇病毒B3(CVB3)建立病毒性心肌炎模型(VMC-WT组和VMC-IL-17A-/-组),同时选取野生型BALB/c小鼠腹腔注射PBS作为正常对照组(WT组)。14 d后取心肌组织作石蜡切片,行HE染色观察病理改变,ELISA测定血清中抗心肌线粒体内膜ADP/ATP载体(ANT)抗体、抗β-肌球蛋白重链(β-MHC)抗体、抗心肌L型钙通道(CACH2)抗体水平。结果与WT组比较,VMC-WT组小鼠抗ANT抗体、抗β-MHC抗体水平升高明显,差异有统计学意义(P<0.01,P<0.05),抗CACH2抗体水平差异无统计学意义(P>0.05);与VMC-WT组比较,VMC-IL-17A-/-组小鼠抗ANT抗体水平降低,差异有统计学意义(P<0.05),抗β-MHC抗体、抗CACH2抗体水平差异无统计学意义(P>0.05)。结论IL-17A参与VMC小鼠血清抗ANT抗体的产生,对抗β-MHC抗体、抗CACH2抗体水平无显著影响。Objective To explore the effect of interleukin-17A (IL-17A) on the serum level of antiheart autoantibodies in mice with viral myocarditis. Methods Male wild-type (WT) and IL-17A-deficient (IL-17A-/- ) BALB/c mice were intraperitoneally injected with Coxsackie virus B3 (CVB3) for establishing VMC models (VMC-WT group and VMC-IL-17A-/- group). Meanwhile, a control group (WT group) of WT mice were established by i. p. administration of phosphate buffered saline (PBS). Paraffin sections of cardiac tissues were made 14 days after CVB3 injection. Myocardial histopathologic changes were evaluated by HE staining. The levels of anti-adenine nucleotide translocator (ANT) autoantibody, anti-β-myosin heavy chain (^-MHC) autoantibody and anti-cardiac L-type calcium channel (CACH2) autoantibody in sere were measured by ELISA. Results Compared with w-r group, the levels of anti-ANT-autoantibody and anti-^-MHC-autoantibody significantly increased in VMC-WT group ( P 〈 0.01, P 〈 0.05 ), while the concentration of anti-CACH2-autoantibody showed no significant difference between WT and VMC-WT groups ( P 〉 0.05). Compared with VMC-WT group, the level of anti-ANT-autoantibody was reduced in VMC-IL-17A -/- group (P 〈 0.05), while the levels of anti-β-MHC-autoantibody and anti-CACH2-autoantibody showed no significantdifference between them (P 〉 0.05 ). Conclusion IL-17A contributed to the secretion of anti-ANT- autoantibody of VMC mice, but had no effect on the secretion of anti-13-MHC-autoantibody and anti-CACH2-autoantibody in VMC mice.
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