激活TAS2R46可以保护肠道屏障免受慢性高葡萄糖的影响
Jiang-Meng Wang1, Sai Tian1, Jing-Yu Duan1
1Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou Medical University, Xuzhou 221004, Jiangsu, China.
Brain, behavior, and immunity
|February 26, 2026
概括
激活苦味受体成员46 (TAS2R46) 信号,改善糖尿病肠道屏障损伤. 这涉及调节SGK3/NF-κB和SNX16/E-cadherin通路,提供治疗潜力.
科学领域:
- 胃肠病学 胃肠病学
- 分子生物学分子生物学
- 内分泌学 在内分泌学.
背景情况:
- 在肠道中苦味受体成员46 (TAS2R46) 的功能在很大程度上是未知的.
- 众所周知,糖尿病会导致肠道屏障受损,但潜在的分子机制需要进一步阐明.
研究的目的:
- 调查TAS2R46信号传递在改善糖尿病肠道屏障损伤中的作用.
- 为了澄清TAS2R46激活影响肠道健康的分子机制.
主要方法:
- 利用糖尿病小鼠模型和高葡萄糖培养的Caco-2细胞.
- 服用了TAS2R46激动剂 (氨酸,氨酸,皮) 并使用TAS2R46阻塞/敲击.
- 进行了PAS和H&E染色,西式涂抹和RNA测序.
主要成果:
- 在糖尿病小鼠和高葡萄糖治疗细胞中,TAS2R46激动剂改善了肠道屏障功能,由增加的紧结蛋白 (Zonula occluden 1,ocludin,E-cadherin) 和改善的形态学证明.
- 通过增加TAS2R46和脂酶Cβ2的表达,证实了TAS2R46信号的激活.
- TAS2R46激活抑制了NF-κB信号传递,并与SGK3和SNX16.6的上调相关.
结论:
- 在糖尿病中,TAS2R46信号激活减轻了肠道屏障损伤.
- 保护作用通过SGK3/NF-κB通路和SNX16/E-cadherin轴进行介导.
- TAS2R46代表了糖尿病肠道并发症的潜在治疗标.
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