Appropriate blood vessel formation is crucial for tendon-bone healing after injury; excessive angiogenesis worsens scar formation, causing chronic pain and dysfunction. This study investigated the regulation of inflammatory angiogenesis during tendon-bone healing. Lipopolysaccharide (LPS)-induced tenocyte inflammation and conditioned medium from these tenocytes were used to treat rat aortic vascular endothelial cells (RAOECs). LPS significantly upregulated NLRP3, TNFα, IL-1β, and VEGFA mRNA and protein levels, along with VEGFA secretion, stimulating RAOEC angiogenesis. Celastrol, a triterpenoid from *Tripterygium wilfordii*, suppressed LPS-induced upregulation of NLRP3 and IL-1β, and VEGFA secretion, inhibiting angiogenesis in RAOECs. In a rotator cuff tear rat model, celastrol administration promoted tendon healing and functional recovery by regulating NLRP3 and VEGFA levels. These findings suggest that inflammation-induced tenocyte injury causes angiogenesis, and celastrol suppresses this angiogenesis to promote tendon-bone healing via the NLRP3 pathway.
