Background
This study aims to evaluate the roles of reactive oxygen species (ROS) generation and inflammasome formation in the development of diabetic rat wound inflammation. Materials and
Conclusion
These data suggest that excessive ROS production contributes to activating NLRP3-IL-1β pathway events and impairs wound healing in a diabetic rat wound model.
Methods
Diabetes was induced in rats by a single intraperitoneal injection of STZ, and a skin wound (2×2 cm2) was produced on the back. Diabetic animals were treated with NAC and Bay 11-7082 to block ROS and the NLRP3 inflammasome, respectively. Total mRNA and protein were isolated from wound tissue and subjected to real-time polymerase chain reaction, Western blot analyses and ELISA. We also assessed the rate of wound closure and time to wound healing.
Results
During healing, the diabetic rat exhibited increased ROS production, NLRP3 inflammasome activation and IL-1β secretion. NAC was responsible for the inhibition of ROS production and NLRP3 inflammasome activation in diabetic rat wounds. We also found that blocking ROS generation improved the impaired healing pattern in diabetic rats and decreased the time for complete skin healing.