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 mechanism regulating inflammatory angiogenesis during tendon-bone healing. Lipopolysaccharide (LPS) induced tenocyte inflammation, and conditioned medium from these inflammatory tenocytes was used to treat rat aortic vascular endothelial cells (RAOECs). LPS significantly upregulated NLRP3, TNF-α, IL-1β, and VEGFA mRNA and protein expression, 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 conditioned medium-induced 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.
