气体传递剂不会阻止由低氧引起的横性离子运输变化,然后再氧化
Rebecca Claßen1, Martin Diener1, Ervice Pouokam1,2
1Institute for Veterinary Physiology and Biochemistry, Justus-Liebig-Universitat Giessen, Giessen, Germany.
Journal of basic and clinical physiology and pharmacology
|January 24, 2024
概括
外源气传递剂在缺氧期间没有保护结肠. 然而,内源硫化 (H2S) 似乎可以保护粘膜完整性和上皮细胞运输功能,这表明低度的H2S具有中等的保护作用.
科学领域:
- 胃肠病学 胃肠病学
- 生理学 生理学 生理学
- 分子生物学分子生物学
背景情况:
- 气体信号分子或气体递质在胃肠道生理学中起着至关重要的作用.
- 在低氧条件下,气体传递物的对结肠离子运输的影响仍然不完全理解.
- 低氧-再氧化循环可能会损害上皮质的完整性和功能.
研究的目的:
- 为了研究外源气体传递剂在低氧/低氧化过程中对结肠离子运输的影响.
- 为了评估这些分子对表皮质的分泌能力后低氧后的影响.
- 阐明内源硫化 (H2S) 在压力期间保护结肠表皮的作用.
主要方法:
- 在老鼠结肠样本上进行了使用室实验.
- 测量了短路电流 (Isc) 和组织电导率 (Gt).
- 使用了各种气传递体供体 (CO,NO,H2S) 和H2S合成的抑制剂.
主要成果:
- 外源的NO,H2S和HNO捐赠者在缺氧之前增加了Isc,但没有改善缺氧诱导的下降.
- 二氧化碳供体CORM-2的分泌能力受损,组织导电性增加,表明有毒性.
- 抑制内源H2S合成导致分泌能力丧失和组织完整性受损.
结论:
- 外源气传递剂在体外低氧/低氧化过程中没有保护结肠离子运输.
- 二氧化碳供体CORM-2对结肠表皮表现出毒性.
- 内生H2S的产生似乎保护了粘膜的完整性和上皮的运输功能,低度在缺氧下显示出适度的保护作用.
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