This study aimed to evaluate the relationship between tumour-necrosis factor-alpha (TNF-α), interleukin (IL)-18, IL-23, IL-35 and Heilcobacter (H) pylori infection with T2DM. A total of 25 healthy subjects and 102 confirmed T2DM patients were enrolled in this study. Diabetic patients were subdivided into six groups according to antidiabetic therapy. Diabetic non-treated patients exhibited a significant elevation in H. Pylori- Ig-G, TNF-α, IL-18, and IL-23 levels, but a noticeable decrease in IL-35 expression was observed compared to healthy controls. Antidiabetic therapy induced a significant decrease in the level of glycosylated hemoglobin (HbA1c), TNF-α, IL-18 and IL-23, while IL-35 expression was upregulated compared to diabetic controls. The results exhibited a positive correlation between H. pylori and HbA1c%, TNF-α, IL-18, and IL-23 values, and also between HbA1c% and TNF-α, IL-18 and IL-23 levels. Therefore, antidiabetic therapy decreases significantly the hyperglycemic state and circulating level of inflammatory cytokines which reflects their potential anti-inflammatory effects.

这项研究旨在评估T2DM的肿瘤坏死因子-α（TNF-α），白介素（IL）-18，IL-23，IL-35和幽门螺杆菌（H）感染之间的关系。共有25名健康受试者和102名确诊的T2DM患者参加了这项研究。根据抗糖尿病治疗方法，将糖尿病患者分为六组。未治疗的糖尿病患者的幽门螺杆菌明显升高-Ig-G，TNF-α，IL-18和IL-23水平，但与健康对照组相比，观察到IL-35表达明显下降。抗糖尿病治疗导致糖基化血红蛋白（HbA1c），TNF-α，IL-18和IL-23的水平显着降低，而与糖尿病对照组相比，IL-35的表达上调。结果显示幽门螺杆菌与HbA1c％，TNF-α，IL-18和IL-23值之间呈正相关，以及HbA1c％与TNF-α，IL-18和IL-23含量之间呈正相关。因此，抗糖尿病治疗显着降低了炎性细胞因子的高血糖状态和循环水平，这反映了它们的潜在抗炎作用。