论文部分内容阅读
目的探讨系统性红斑狼疮(SLF)患者中p16基因的甲基化状态及其在发病机制中的作用。方法检测45例SLE患者及20例健康对照者血浆DNA甲基化状态。应用甲基化特异PcR(MSP) 方法检测p16基因启动子区甲基化状态,并分析与临床表现及常规实验室检查结果之间的关联。结果在SLE患者血浆DNA中p16基因呈现高甲基化状态,占64.44%(29/45),而健康对照组中只有1例检测到p16基因高甲基化(1/20,5%),两组间差异有统计学意义(x2=19.69,P<0.01)。活动期SLE组p16基因呈高甲基化状态者所占比率83.33%(20/24),比非活动期SLE组42.85%,(9/21)高,差异也有统计学意义(x2=8.01;P<0.01)。但初发SLE组p16基因呈高甲基化状态者所占比例(71.43%,15/21)与复发SLE 组(58.33%,14/24)相比差异无统计学意义(P=0.37)。具有下列临床表现的SLE患者其血浆p16基因高甲基化状态者所占比率相对较高:关节炎(57.5%,15/26),白细胞减少(42.3%,11/26),血沉增快(56%,14/ 25)。结论活动期SLE患者血浆DNA p16基因启动子区呈现明显高甲基化状态,并与关节炎、白细胞减少及血沉增快等临床表现相关;提示p16基因启动子区高甲基化可能在SLE的发病机制中起作用。
Objective To investigate the methylation status of p16 gene and its role in the pathogenesis of systemic lupus erythematosus (SLF). Methods Plasma DNA methylation status was examined in 45 SLE patients and 20 healthy controls. Methylation specific PcR (MSP) was used to detect the methylation status of p16 gene promoter region, and its correlation with clinical manifestations and routine laboratory test results was analyzed. Results In the plasma DNA of SLE patients, the p16 gene was hypermethylated (64.44%, 29/45), but only one case of hypermethylation (1/20, 5%) of p16 gene was detected in healthy controls. The difference between the two groups There was statistical significance (x2 = 19.69, P <0.01). Active SLE group p16 gene hypermethylation status accounted for 83.33% (20/24), than non-active SLE group 42.85%, (9/21), the difference was statistically significant (x2 = 8.01; P < 0.01). However, the proportion of patients with newly diagnosed SLE with p16 hypermethylation (71.43%, 15/21) was not significantly different from that in patients with recurrent SLE (58.33%, 14/24) (P = 0.37). The percentage of hypermethylated plasma p16 gene was higher in patients with SLE with the following clinical manifestations: arthritis (57.5%, 15/26), leukopenia (42.3%, 11/26), erythrocyte sedimentation rate (56% , 14/25). Conclusions The promoter region of plasma DNA p16 gene in active SLE patients is obviously hypermethylated and is associated with the clinical manifestations such as arthritis, leukopenia and erythrocyte sedimentation rate. It suggests that hypermethylation of p16 gene promoter may play an important role in the pathogenesis of SLE effect.