Diabetes is associated with an increased risk of cardio-vascular disease. A decrease in the number and functionality of endothelial progenitor cells (EPCs) leads to reduced endothelial repair and the development of cardiovascular disease. The aim of the present study was to explore the effect and underlying mechanisms of nuclear factor erythroid 2-related factor 2 (Nrf2) on EPC dysfunction caused by diabetic mellitus. The biological functions of EPCs in streptozotocin-induced diabetic mice were evaluated, including migration, proliferation, angiogenesis and the secretion of vascular endothelial growth factor (VEGF), stromal-derived growth factor (SDF) and nitric oxide (NO). Oxidative stress levels in diabetic EPCs were also assessed by detecting intracellular reactive oxygen species (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA). EPC senescence was evaluated by measuring p16 and b-gal expression and observing the senescence-associated secretory phenotype. In addition, the function of EPCs and level of oxidative stress were assessed following Nrf2 silencing or activation. Nrf2 silencing resulted in a decrease of EPC biological functions, accelerated cell senescence and increased oxidative stress, as indicated by ROS and MDA upregulation accompanied with decreased SOD activity. Furthermore, Nrf2 silencing inhibited migration, proliferation and secretion in EPCs, while it increased oxidative stress and cell senescence. Nrf2 activation protected diabetic EPCs against the effects of oxidative stress and cell senescence, ameliorating the biological dysfunction of EPCs derived from mice with diabetes. In conclusion, Nrf2 overexpression protected against oxidative stress-induced functional damage in EPCs derived from diabetic mice by regulating cell senescence.

F-18 fluorodeoxyglucose (FDG) positron emission tomography/computerized tomography (PET/CT) is considered to be the most beneficial imaging method for staging patients with lymphoma. Whether maximum standardized uptake value (SUVmax), metabolic tumor volume (MTV) and total lesion glycolysis (TLG) acquired from F-18 FDG PET/CT are predictors of prognosis of diffuse large B cell lymphoma (DLBCL) is controversial, with some studies concluding that it is and others concluding the opposite. Therefore, a systematic review was performed to explore the relationship of F-18 FDG PET/CT quantization parameters with the prognosis of DLBCL. Seven trials with a total of 703 DLBCL patients were included for analysis. Hazard ratios (HRs) for progression-free survival (PFS) and overall survival (OS), and odds ratios (ORs) for 3-year PFS and OS were pooled using the STATA package. Combined results suggested a strong link between the high SUVmax, MTV and TLG values and the poor 3-year PFS with ORs of 2.59, 3.69 and 2.29, respectively. Similarly, high MTV and TLG values unfavorably influenced the 3-year OS with ORs of 5.40 and 2.19, respectively. The pooled results also showed that high SUVmax and MTV were negative predictors of PFS with HRs of 1.61 (p = 0.038) and 2.18 (p = 0.000), respectively. The TLG value was not predictive of PFS. And for OS, only high MTV was a strong predictor of poor prognosis in DLBCL with HR 2.99 (p = 0.000). Our results suggested that SUVmax and MTV may be significant prognostic markers for PFS and MTV may be the only predictor for OS in DLBCL.

Aging is associated with an increased risk of cardiovascular disease. Numerical and functional declines in endothelial progenitor cells (EPCs) limit their capacity for endothelial repair and promote the development of cardiovascular disease. We explored the effects of nuclear factor (erythroid-derived 2)-like 2 (NRF2) on EPC activity during aging. Both in vitro and in vivo, the biological functioning of EPCs decreased with aging. The expression of NRF2 and its target genes (Ho-1, Nqo-1 and Trx) also declined with aging, while Nod-like receptor protein 3 (NLRP3) expression increased. Aging was associated with oxidative stress, as evidenced by increased reactive oxygen species and malondialdehyde levels and reduced superoxide dismutase activity. Nrf2 silencing impaired the functioning of EPCs and induced oxidative stress in EPCs from young mice. On the other hand, NRF2 activation in EPCs from aged mice protected these cells against oxidative stress, ameliorated their biological dysfunction and downregulated the NLRP3 inflammasome. These findings suggest NRF2 can prevent the functional damage of EPCs and downregulate the NLRP3 inflammasome through NF-κB signaling.