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松蛋白缓解UVB诱导的HaCaT细胞和皮肤损伤

Kaiyue Liu¹, Chenxu Zhao¹, Ke Zhang¹

¹College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.

Molecules (Basel, Switzerland)

|September 14, 2024

概括

角蛋白有效地修复UVB诱导的皮肤光损伤. 它通过调节关键细胞通路来增强原蛋白和氨酸,减少氧化应激和炎症.

科学领域:

皮肤病学皮肤病学
生物化学生物化学
细胞生物学细胞生物学

背景情况:

紫外线B (UVB) 辐射通过氧化应激和炎症引起皮肤光损伤.
皮洛斯角的提取物以其抗炎和抗氧化特性而闻名.

研究的目的:

调查角蛋白 (PAP) 在修复UVB诱导的光损伤中的机制.
为了评估PAP对HaCaT细胞和ICR小鼠皮肤的影响.

主要方法:

评估了PAP对UVB照射HaCaT细胞中的I型原蛋白和氨酸表达的影响.
在体外测量了活性氧物种 (ROS) 生产和氧化应激标志物.
评估了PAP在暴露于UVB的ICR小鼠上的局部应用效应,分析了炎症性细胞因子 (IL-1β,IL-6,TNF-α) 和氧化应激标志物.
研究了MAPK和TGF-β/Smad通路的参与.

主要成果:

PAP在HaCaT细胞中增加了I型原蛋白和氨酸的合成.
在实验室中,PAP抑制了ROS的产生和氧化应激.
在小鼠中,局部PAP应用减少了UVB诱导的皮肤炎症和氧化应激.
PAP调节的白素-1β,白素-6和瘤亡因子-α水平.
修复机制涉及MAPK和TGF-β/Smad通路.

结论:

角蛋白在修复UVB诱导的皮肤光损伤方面表现出显著的有效性.
通过增强原蛋白和氨酸的产生,减轻氧化应激和减少炎症来提高PAP的功能.
保护作用通过MAPK和TGF-β/Smad信号通路进行介导.

关键词:

这些细胞是Hacat细胞.紫外线 (UVB) 是一种UVB.皮洛斯·安特勒 (pilose antler) 是一家在美国的公司.皮肤损伤皮肤损伤

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