Hydrogen sulfide (H 2S) is an important messenger for its strong anti-inflammatory effects, which may be involved in multiple
cardiovascular diseases. In our previous study, we revealed that H 2S attenuated diabetes-accelerated
atherosclerosis through suppressing oxidative stress. Here we report that
GYY4137, a H 2S donor, reduced the plaque formation of aortic roots and the levels of both intercellular
cell adhesion molecule 1 (ICAM1) and
vascular cell adhesion molecule 1 (VCAM1) in diabetes-accelerated atherosclerotic cells and mouse models. The inflammatory factors of TNF-α, IL-1β,
IL-6, and MCP1 were also significantly reduced by
GYY4137. Mechanically,
GYY4137 suppressed the activation of pyrin domain containing
protein 3 (NLRP3)
inflammasome in diabetes-accelerated
atherosclerosis conditions. Upon knockdown of NLRP3, the increase of ICAM1 and VCAM1 caused by high
glucose and
oxLDL could be reversed, indicating that H 2S protected the endothelium by inhibiting the activity of NLRP3
inflammasome. In conclusion, our study indicates that
GYY4137 effectively protects against the development of diabetes-accelerated
atherosclerosis by inhibiting
inflammasome activation.