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目的研究DNaseⅠ在多发性肌炎和皮肌炎发病机制中的作用。方法选择2011年12月至2012年10月在中日友好医院风湿免疫科住院患者中符合多发性肌炎(PM)/皮肌炎(DM)诊断标准的61例患者作为病例组。同期选择48例健康成年人作为对照组。辐射状酶扩散法测定血浆Ⅰ型脱氧核糖核酸酶(DNaseⅠ)活性,并与患者血清学指标进行相关性分析。在DNaseⅠ活性受损的患者血浆中添加外源性DNaseⅠ和微球菌核酸酶(MNase),进一步分析DNaseⅠ活性受损的原因。结果 DNaseⅠ活性在PM/DM组为(0.3353±0.1894)U/ml,显著低于健康对照组[(0.5441±0.2536)U/ml,P<0.0001]。36例DNaseⅠ活性显著受损的患者血浆中添加外源性重组DNaseⅠ后,11例患者的血浆不能明显恢复DNaseⅠ活性,而添加MNase后,患者血浆对底物dsDNA的降解完全恢复,说明这些患者血浆中存在DNaseⅠ的特异性抑制剂。相关性分析提示DNaseⅠ活性与血清球蛋白(r=0.366,P=0.005)和IgG(r=0.322,P=0.012)呈正相关。结论 PM/DM患者血浆DNaseⅠ活性显著低于健康对照;部分PM/DM患者血浆中存在DNaseⅠ的特异性抑制剂;DNaseⅠ的活性受损可能在PM/DM发病中起一定作用。
Objective To study the role of DNase Ⅰ in the pathogenesis of polymyositis and dermatomyositis. Methods From December 2011 to October 2012, 61 patients with rheumatoid arthritis who met the criteria of polymyositis (PM) / dermatomyositis (DM) in the Sino-Japanese Friendship Hospital were selected as the case group. In the same period, 48 healthy adults were selected as the control group. The activity of DNase Ⅰ in plasma was detected by the radionuclide diffusion method and the correlation with the serological parameters of patients was analyzed. Exogenous DNase I and micrococcal nuclease (MNase) were added to the plasma of patients with impaired DNase I activity to further analyze the cause of impaired DNase I activity. Results The DNase Ⅰ activity in the PM / DM group was (0.3353 ± 0.1894) U / ml, significantly lower than that in the healthy control [(0.5441 ± 0.2536) U / ml, P <0.0001]. Thirty-six patients with DNase Ⅰ activity were significantly damaged after addition of exogenous recombinant DNase Ⅰ, the plasma of 11 patients did not recover DNase Ⅰ activity significantly. However, the addition of MNase completely restored the degradation of dsDNA in the plasma of patients, indicating that plasma There is a DNase I-specific inhibitor. Correlation analysis indicated that DNase I activity was positively correlated with serum globulin (r = 0.366, P = 0.005) and IgG (r = 0.322, P = 0.012) Conclusions Plasma DNase I activity in patients with PM / DM is significantly lower than that in healthy controls. Some patients with PM / DM have DNase I specific inhibitors. The activity of DNase I may play a role in the pathogenesis of PM / DM.