Abstract Title:

β-Elemene Attenuates Fibrosis after Esophageal Endoscopic Submucosal DissectionModulating the HIF-1α/HK2/p38-MAPK Signaling Axis.

Abstract Source:

ACS Biomater Sci Eng. 2021 07 12 ;7(7):3399-3408. Epub 2021 Jun 10. PMID: 34109793

Abstract Author(s):

Caifa Hong, Huie Zhuang, Baorang Cai, Jiangmu Chen, Sifu Huang, Taiyong Fang

Article Affiliation:

Caifa Hong


Esophageal fibrosis and stricture after endoscopic submucosal dissection (ESD) are serious postoperative complications. Previous evidence has highlighted an anticancer role ofβ-elemene in esophageal squamous cell carcinoma. This study put forward a hypothesis on the inhibitory effect of β-elemene on esophageal fibrosis after ESD and aimed to elaborate the underlying mechanisms. Our initial network pharmacology analyses determined hypoxia-inducible factor-1alpha (HIF-1α), hexokinase 2 (HK2), and p38MAPK in association with the effect of β-elemene. We validated that the levels of HIF-1α, HK2, and p-p38MAPK were elevated in esophageal granulation tissue after ESD and corresponding fibroblasts. Esophageal fibroblasts were treated with β-elemene of gradient concentrations. The results indicated that β-elemene repressed the proliferation of esophageal fibroblasts and the levels of fibrosis-related factors. Further, β-elemene inhibited HIF-1α expression leading to restricted proliferation and augmented apoptosis of fibroblasts. HIF-1α induced p38MAPK phosphorylation by activating the HK2 transcription and consequently accelerated fibroblast proliferation. Together, β-elemene diminished HIF-1α expression and impaired the HK2-mediated p38MAPK phosphorylation, thereby repressing the esophageal fibrosis.

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