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Updated: Dec 30, 2025
A Protocol for Constructing a Rat Wound Model of Type 1 Diabetes
Published on: February 17, 2023
ROS-activated NLRP3 inflammasome initiates inflammation in delayed wound healing in diabetic rats
Jiezhi Dai1, Xiaotian Zhang1, Yanmao Wang1
1Department of Orthopedic Surgery, Shanghai Sixth People's Hospital, Jiaotong University Shanghai, China.
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 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.
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.
Insights
Diabetic wound inflammation involves excessive reactive oxygen species (ROS) and NLRP3 inflammasome activation. Blocking ROS and inflammasome formation accelerates diabetic wound healing in rats.
Area of Science:
- Biomedical Science
- Wound Healing Research
- Diabetic Complications
Background:
- Diabetic wound inflammation is a significant clinical challenge.
- The roles of reactive oxygen species (ROS) and inflammasome activation in this process require further elucidation.
Purpose of the Study:
- To investigate the involvement of ROS generation and inflammasome formation in diabetic rat wound inflammation.
- To evaluate the therapeutic potential of targeting these pathways.
Main Methods:
- Diabetes induced in rats using streptozotocin (STZ).
- Skin wounds created and treated with ROS inhibitor (NAC) and NLRP3 inflammasome inhibitor (Bay 11-7082).
- Gene expression, protein levels, and wound healing rates were analyzed.
Main Results:
- Diabetic rat wounds showed increased ROS production, NLRP3 inflammasome activation, and IL-1β secretion.
- NAC treatment inhibited ROS and NLRP3 inflammasome activation.
- Blocking ROS improved wound healing and reduced healing time in diabetic rats.
Conclusions:
- Excessive ROS production is a key contributor to NLRP3-IL-1β pathway activation in diabetic wounds.
- Targeting ROS offers a promising strategy to improve wound healing in diabetic patients.
