Purple sweet potato color (PSPC), flavonoids isolated from purple sweet potato, has been well demonstrated for the pharmacological properties. In the present study, we attempt to explore whether the antisenescence was involved in PSPC-mediated protection against endothelium dysfunction in type 2 diabetes mellitus (T2DM) and, if involved, what are the possible mechanisms. The results showed that atherogenesis and endothelial senescence in the thoracic aorta were promoted in mice with prediabetes; meanwhile, PSPC attenuated the deterioration of vascular vessel and inhibited the endothelial senescence. Diabetes mellitus is a documented high-risk factor for the development of atherosclerosis. Studies show that D-galactose (D-gal) promotes endothelial cell senescence in vitro. In our study, we have determined that PSPC could suppress the D-gal-induced premature senescence and the abnormal endothelial function, discovered in the early stages of atherosclerosis induced by T2DM. We have discovered that the PSPC down-regulates reactive oxygen species (ROS) accumulation and the NLRP3 inflammasome functions. Furthermore, the premature senescence induced by D-gal was inhibited after attenuation of ROS and deactivation of NLRP3 inflammasomes. However, once the NLRP3 inflammasomes are overactivated, PSPC could not restrain cell senescence. These data imply that the beneficial effects of PSPC on diabetes-induced endothelial dysfunction and senescence are mediated through ROS and NLRP3 signaling pathways, suggesting a potential target for the prevention of endothelial senescence-related cardiovascular diseases.
Keywords: Endothelial cells; NLRP3 inflammasome; Premature senescence; Purple sweet potato color; Type 2 diabetes mellitus.
Copyright © 2015. Published by Elsevier Inc.