ArticleWorld journal of gastroenterology2025
Celastrol alleviates esophageal stricture in rats by inhibiting NLR family pyrin domain containing 3 activation.
Article in World journal of gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThe role of NLR family pyrin domain containing 3 (NLRP3) in post-endoscopic submucosal dissection (ESD) esophageal stricture remains incompletely understood. The effect of celastrol (CEL) on the prevention of esophageal strictures has not yet been investigated.
aimTo explore the effect of CEL on the prevention of esophageal stricture in rats.
methodsNLRP3, interleukin (IL)-1β, and IL-18 mRNA levels were measured in patients' tissues after esophageal ESD. NLRP3 expression in esophageal fibroblasts was determined using immunohistochemistry and immunofluorescence staining. Lentiviral transfection was used to induce NLRP3 overexpression and thioredoxin reductase 1 (TXNRD1) silencing. The CCK8 assay was used to determine the optimal CEL concentration. Reactive oxygen species (ROS) generation was detected
resultsThe mRNA levels of NLRP3 and IL-1β were higher in human tissues from the ESD resection bed than in normal esophageal mucosa. NLRP3 overexpression in primary rat esophageal fibroblasts led to high collagen 1 expression. Thus, NLRP3 participated in esophageal inflammation and tissue repair after ESD. Comparable to prednisolone, CEL significantly inhibited NLRP3 activation
conclusionCEL is a promising alternative therapeutic agent for the prevention of post-ESD esophageal strictures.
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