AGE/巨/TNF-α通路的变化会影响KK-Ay/Tajcl小鼠老化过程中的皮肤干燥
Keiichi Hiramoto1, Masashi Imai1, Shota Tanaka1
1Department of Pharmaceutical Sciences, Suzuka University of Medical Science, Suzuka 513-8670, Japan.
Life (Basel, Switzerland)
|June 28, 2023
概括
2型糖尿病的皮肤干燥会随着年龄的增长而恶化,原因是晚期糖化终产物 (AGE),前列腺素E2 (PGE2) 和瘤缩因子-α (TNF-α) 的增加. 这些因素,加上 AGE (RAGE) 受体升高和原减少,导致与年龄相关的皮肤干燥.
科学领域:
- 皮肤病学 皮肤病学
- 内分泌学 在内分泌学.
- 衰老研究研究 衰老研究
背景情况:
- 皮肤干燥是2型糖尿病的常见并发症.
- 糖尿病中衰老和皮肤干燥增加之间的机制尚未完全理解.
研究的目的:
- 在2型糖尿病小鼠模型中研究衰老对皮肤干燥的影响.
- 为了阐明参与糖尿病小鼠与年龄相关的皮肤干燥的分子途径.
主要方法:
- 使用了不同年龄 (10,27,40,50周) 的KK-Ay/TaJcl小鼠.
- 评估了皮肤干燥,先进的糖化终产物 (AGE),前列腺素E2 (PGE2),瘤缩因子-α (TNF-α),AGE (RAGE) 表达受体,巨细胞透和原水平.
主要成果:
- 在糖尿病小鼠中,皮肤干燥的严重程度随着年龄的增长而增加.
- 在老年糖尿病小鼠皮肤中观察到高AGE,PGE2和TNF-α水平.
- 在老年糖尿病人皮肤中注意到RAGE表达的增加,巨细胞的透和原蛋白的减少.
结论:
- 在2型糖尿病中,皮肤干燥会随着年龄的增长而加剧.
- AGE/RAGE/PGE2和TNF-α通路在糖尿病小鼠的与年龄相关的皮肤干燥中发挥了关键作用.
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