论文部分内容阅读
目的研究瘦素(Leptin)在系统性红斑狼疮(SLE)患者中表达情况及与疾病活动度、临床和实验室指标及CD4~+CD25~+Foxp3~+Tregs的关系,探讨Leptin对Treg调节作用及对SLE发病的影响。方法选择47例女性SLE患者作为SLE组,另选择年龄、体质量指数与实验组相当的健康体检者25例作为健康组,采用ELISA方法和流式细胞学技术(FACS)测定2组血浆Leptin水平及外周血Tregs百分率,比较SLE组不同疾病活动度患者Leptin水平并分析Leptin与疾病活动评分(SLEDAI)、临床表现、实验室指标及外周血Tregs的相关性。分离SLE患者外周血单个核细胞(PBMC),FACS分析在有/无抗Leptin条件下体外培养40h及80h Tregs百分率。结果 SLE组血浆Leptin水平显著高于健康组(P<0.05);SLE患者中度活动组及重度活动组血浆Leptin水平均高于健康组(P均<0.05),且重度活动组Leptin水平明显高于中度及轻度活动组(P均<0.05);SLE患者血浆Leptin水平与SLEDAI呈正相关(r=0.316 2,P=0.030 4),而与外周血Tregs呈明显负相关(r=0.288 8,P=0.049 0);健康组血浆Leptin水平与外周血Tregs则无明显相关性(r=0.121 9,P=0.561 5)。体外实验中抗Leptin处理后Tregs数量显著增加(P<0.05)。结论 SLE患者血清Leptin水平显著升高,在某种程度上疾病活动程度越高,其血清Leptin水平越高;Leptin可能通过抑制Tregs增殖参与SLE发病。
Objective To investigate the expression of leptin in patients with systemic lupus erythematosus (SLE) and its relationship with disease activity, clinical and laboratory parameters and CD4 ~ + CD25 ~ + Foxp3 ~ + Tregs, and investigate the role of Leptin in regulating Treg And the impact on the incidence of SLE. Methods Forty-seven female SLE patients were selected as SLE group. Another 25 healthy subjects with age and body mass index as the experimental group were selected as healthy group. The plasma Leptin levels were measured by ELISA and flow cytometry (FACS) And the percentage of Tregs in peripheral blood. The levels of Leptin in SLE patients with different disease activity were compared. The correlation between Leptin and SLEDAI, clinical manifestations, laboratory parameters and Tregs in peripheral blood were also analyzed. Peripheral blood mononuclear cells (PBMCs) were isolated from patients with SLE. The percentages of Tregs cultured in vitro with or without anti-Leptin for 40h and 80h were analyzed by FACS. Results The level of Leptin in SLE group was significantly higher than that in healthy group (P <0.05). The level of Leptin in SLE group was significantly higher than that in healthy group (P <0.05), and the level of Leptin in severe active group was significantly higher (P <0.05). The level of Leptin in SLE patients was positively correlated with SLEDAI (r = 0.316 2, P = 0.030 4), but negatively correlated with Tregs in peripheral blood (r = 0.288 8 , P = 0.049 0). There was no significant correlation between Leptin level in plasma and Tregs in peripheral blood (r = 0.121 9, P = 0.561 5). In vitro, the number of Tregs after anti-Leptin treatment increased significantly (P <0.05). Conclusions Serum Leptin levels in patients with SLE are significantly increased. To some extent, the higher the degree of disease activity is, the higher the serum Leptin level is. Leptin may be involved in the pathogenesis of SLE by inhibiting the proliferation of Tregs.