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目的探讨新发2型糖尿病患者外周血单核细胞(PMNC)中NF-κB的活性变化。方法选择2004年10月至2006年1月中山大学附属第二医院体检健康成人30名,新发2型糖尿病患者30例。免疫印迹分析检测两组人群外周血单核细胞(PMNC)中核因子κB(NF-κB)P65(Ser536)的磷酸化水平,肌动蛋白(actin)作为内参。两组人群血清超敏C反应蛋白(hs-CRP)采用酶联免疫吸附(ELISA)法测定。结果2型糖尿病组患者PBMC中NF-κBP65(Ser536)磷酸化水平高于对照组[0.85(95%可信区间为0.49~1.02)对0.47(95%可信区间为0.26~0.67),P<0.05];糖尿病组患者的hs-CRP显著高于对照组[2.00mg/L(95%可信区间为1.21~4.60)对0.83mg/L(95%可信区间为0.10~1.75),P<0.01],C-反应蛋白(CRP)以中位数表示;在糖尿病组,磷酸化NF-κBP65(Ser536)与log(CRP)呈正相关(r=0.351,P<0.05),log(CRP)与体重指数(BMI)、腰围(W)、稳态模型法估计的胰岛素抵抗指数(HOMA-IR)、糖基化血红蛋白(GHbA1c)呈正相关。结论提示2型糖尿病患者PMNC处于炎症状态,其中NF-κB活性的升高可能影响胰岛素抵抗和动脉粥样硬化的形成。
Objective To investigate the changes of NF-κB activity in peripheral blood mononuclear cells (PMNC) of newly diagnosed type 2 diabetic patients. Methods From October 2004 to January 2006, the Second Affiliated Hospital of Sun Yat-sen Medical Examination 30 healthy adults, 30 newly diagnosed type 2 diabetic patients. The level of phosphorylation of NF-κB P65 (Ser536) in peripheral blood mononuclear cells (PMNC) was detected by Western blot analysis. Actin was used as an internal control. Serum high-sensitivity C-reactive protein (hs-CRP) was measured by enzyme-linked immunosorbent assay (ELISA) in both groups. Results The phosphorylation level of NF-κB P65 (Ser536) in PBMC of type 2 diabetic patients was significantly higher than that of the control group [0.85 (95% confidence interval 0.49-1.02) vs 0.47 (95% confidence interval 0.26-0.67), P < 0.05]. The hs-CRP in patients with diabetes mellitus was significantly higher than that in the control group [2.00mg / L (95% confidence interval 1.21-4.60) vs 0.83mg / L (95% confidence interval 0.10 ~ 1.75), P < (P <0.05). There was a significant positive correlation between log (CRP) and log (CRP) in the diabetic group Body mass index (BMI), waist circumference (W), HOMA-IR and GHbA1c estimated by steady-state model were positively correlated. Conclusions The PMNC in patients with type 2 diabetes mellitus is in an inflammatory state, and the increase of NF-κB activity may affect the formation of insulin resistance and atherosclerosis.