论文部分内容阅读
目的研究T2DM患者外周血CD14+CD16+单核细胞数和血清IL-6、TGF-β的水平,及患者血清和IL-6孵育的THP-1单核细胞源性巨噬细胞STAT3、p-STAT3的蛋白表达,以了解炎症性免疫反应在T2DM大血管病变中的可能作用。方法对42例T2DM(T2DM组)患者和35名健康体检者(NC组)采用外周血流式细胞术检测外周血单核细胞CD14+CD16+的表达,并分离其外周血血清。采用ELISA检测血清中细胞因子IL-6及TGF-β的浓度,免疫比浊法检测血清中高敏C反应蛋白(hsC-RP)水平,血清和IL-6孵育THP-1单核细胞源性巨噬细胞,采用Western blot检测其STAT3和p-STAT3的蛋白表达。结果 T2DM组外周血CD14+CD16+单核细胞数高于NC组(P<0.01),且与血清hsC-RP和IL-6水平呈正相关(r=0.462、0.495,P<0.01),与TGF-β水平无相关性(P>0.05)。T2DM组24hUAlb水平、大血管病变发病率及THP-1单核细胞源性巨噬细胞p-STAT3的蛋白表达均高于NC组(P<0.01)。结论 T2DM患者体内可能存在单核/巨噬细胞功能异常,其可能参与了T2DM患者体内免疫炎症反应,从而导致了T2DM及其血管病变的发生发展,作用机制可能与STAT3信号通路的激活有关。
Objective To investigate the levels of CD14 + CD16 + monocytes and serum levels of IL-6 and TGF-β in peripheral blood of patients with T2DM and STAT3 and p-STAT3 of THP-1 monocyte-derived macrophages incubated with serum and IL-6 Protein expression in order to understand the possible role of inflammatory immune response in T2DM macroangiopathy. Methods 42 cases of T2DM (T2DM group) and 35 healthy subjects (NC group) were detected by peripheral blood flow cytometry of peripheral blood mononuclear cells CD14 + CD16 + expression, and the separation of peripheral blood serum. Serum concentrations of IL-6 and TGF-β were measured by ELISA. Serum levels of hsC-RP were measured by immunoturbidimetric assay. Serum and IL-6 were incubated with THP-1 monocyte-derived macrophages Western blot was used to detect the protein expression of STAT3 and p-STAT3. Results The number of CD14 + CD16 + monocytes in T2DM group was significantly higher than that in NC group (P <0.01), and positively correlated with the levels of serum hsC-RP and IL-6 (r = 0.462,0.495, P <0.01) β level no correlation (P> 0.05). The level of 24hUAlb, the incidence of macrovascular disease and the protein expression of p-STAT3 in THP-1 monocyte-derived macrophages in T2DM group were higher than those in NC group (P <0.01). Conclusions There may be dysfunction of monocytes / macrophages in T2DM patients, which may be involved in the immune inflammatory reaction in T2DM patients, leading to the development of T2DM and its vascular pathology. The possible mechanism may be related to the activation of STAT3 signaling pathway.