榄香烯
癌症研究
成纤维细胞
食管癌
纤维化
细胞凋亡
MAPK/ERK通路
医学
磷酸化
病理
化学
内科学
生物
癌症
细胞生物学
体外
生物化学
作者
Caifa Hong,Huie Zhuang,Baorang Cai,Jiangmu Chen,Sifu Huang,Taiyong Fang
出处
期刊:ACS Biomaterials Science & Engineering
[American Chemical Society]
日期:2021-06-10
卷期号:7 (7): 3399-3408
被引量:3
标识
DOI:10.1021/acsbiomaterials.1c00047
摘要
Esophageal fibrosis and stricture after endoscopic submucosal dissection (ESD) are serious postoperative complications. Previous evidence has highlighted an anticancer role of β-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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