Biros Erik, Vangaveti Venkat, Malabu Usman
Translational Research in Endocrinology and Diabetes, College of Medicine and Dentistry, James Cook University, 1 James Cook Drive, Townsville, QLD, 4811, Australia.
Townsville University Hospital, Townsville, Australia.
Diabetol Metab Syndr. 2024 Aug 22;16(1):204. doi: 10.1186/s13098-024-01444-3.
The study aimed to investigate the molecular mechanisms underlying the effects of Vildagliptin on the healing of diabetic foot ulcers (DFUs). The research compared patients who received 12 weeks of Vildagliptin treatment to those who did not. Various molecular markers associated with wound healing were measured. Wound fluid samples were collected from DFUs using a filter paper absorption technique, and total RNA was extracted for quantitative real-time PCR (qPCR). The results showed that the autophagy marker NUP62 was significantly downregulated in the Vildagliptin group at week 12 compared to baseline (median expression 0.57 vs. 1.28; P = 0.0234). No significant change was observed in the placebo group (median expression 1.61 vs. 1.48; P = 0.9102). Both groups showed substantial downregulation of RIPK3, a necroptosis marker, at week 12 compared to their respective baselines. In addition to its effects on blood sugar levels, Vildagliptin may promote DFU healing by reducing autophagy in patients with diabetes.
该研究旨在探究维格列汀对糖尿病足溃疡（DFU）愈合影响的分子机制。该研究将接受12周维格列汀治疗的患者与未接受治疗的患者进行了比较。测量了与伤口愈合相关的各种分子标志物。使用滤纸吸收技术从DFU收集伤口液样本，并提取总RNA用于定量实时PCR（qPCR）。结果显示，与基线相比，维格列汀组在第12周时自噬标志物NUP62显著下调（中位表达0.57对1.28；P = 0.0234）。安慰剂组未观察到显著变化（中位表达1.61对1.48；P = 0.9102）。与各自基线相比，两组在第12周时坏死性凋亡标志物RIPK3均显著下调。除了对血糖水平的影响外，维格列汀可能通过减少糖尿病患者的自噬来促进DFU愈合。
