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陈氧胆酸通过诱导亡和FXR激活引发胃粘膜损伤
Shuaijun Peng1,2, Ruiqin Sun3, Hui Liu1,2
1Collaborative Innovation Center for Research and Development on the Whole Industry Chain of Yu-Yao in Henan Province, Henan University of Chinese Medicine, Zhengzhou, China.
陈氧胆酸 (CDCA) 通过诱导亡和激活Farnesoid X受体 (FXR) 引起胃粘膜损伤. 抑制FXR可能为胆酸诱导的胃损伤提供治疗策略.
科学领域:
- 胃肠病学 胃肠病学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 胃粘膜损伤与炎症和等胃肠道疾病有关.
- 胆汁酸有助于粘膜损伤,但陈氧胆酸 (CDCA) 的具体作用尚不清楚.
研究的目的:
- 研究CDCA在胃粘膜损伤中的作用.
- 阐明涉及亡和FXR激活的机制.
- 确定胃粘膜疾病的潜在治疗点.
主要方法:
- 向小鼠服用CDCA,评估生理和病理变化.
- 分析基因表达 (Bax,Bcl-2,Cdx2) 通过RT-PCR和西式涂抹.
- 在体外评估了GES-1细胞活力,细胞亡和FXR抑制效应.
主要成果:
- 在小鼠中,CDCA诱导体重减轻,摄入量减少,胃损伤和肠道代谢.
- 在GES-1细胞中,CDCA上调了Bax和CDX2,降低了Bcl-2的调节,并增加了GES-1细胞的亡.
- 抑制FXR可以逆转CDCA诱导的细胞损伤和细胞亡.
结论:
- 通过亡和FXR激活,CDCA会诱导胃粘膜损伤.
- FXR是胆汁酸相关的胃粘膜损伤的潜在治疗标.
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