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Anti-Aging Effect and Mechanism of Proanthocyanidins Extracted from Sea buckthorn on Hydrogen Peroxide-Induced Aging Human Skin Fibroblasts
Antioxidants ( IF 7 ) Pub Date : 2022-09-25 , DOI: 10.3390/antiox11101900
Xinying Liu 1 , Yi Xing 1 , Michael Yuen 2 , Tina Yuen 2 , Hywel Yuen 2 , Qiang Peng 1
Affiliation  

Oxidative stress is the leading cause of skin aging damage. Excessive accumulation of reactive oxygen species (ROS) in cells induced by hydrogen peroxide (H2O2) triggers a decrease in collagen synthesis and an increase in collagen degradation, which are biomarkers of skin aging. We evaluated the potential protective mechanism of Sea buckthorn proanthocyanidins (SBP) against the oxidative stress-induced skin aging process from multiple aspects. We treated human skin fibroblasts (HSFs) with 300 µmoL/L of H2O2 for 24 h, followed by 25, 50, and 100 µg/mL of SBP for 24 h. The results showed that SBP could enhance the activities of superoxide dismutase (SOD) and glutathione (GSH), effectively remove excess ROS, and significantly improve the changes in cell morphology and viability caused by excessive ROS in skin cells. In addition, SBP could promote the synthesis of Col I in aging HSFs through the TGF-β1/Smads pathway and inhibit the degradation of Col I by regulating the MMPs/TIMPs system, thereby maintaining the stability of the ECM structure to achieve anti-aging purposes. Finally, we studied the migration ability of SBP, and the results showed that 100 µg/mL of SBP was most conducive to the cell migration of senescent cells, laying a foundation for follow-up animal experiments. These results will increase the application value of SBP in the cosmetic and antioxidative functional food industries.

中文翻译:

沙棘提取物原花青素对过氧化氢诱导衰老人皮肤成纤维细胞的抗衰老作用及机制

氧化应激是皮肤老化损伤的主要原因。由过氧化氢 (H 2 O 2 )诱导的细胞中活性氧 (ROS) 的过度积累会引发胶原蛋白合成减少和胶原蛋白降解增加,这些都是皮肤老化的生物标志物。我们从多个方面评估了沙棘原花青素 (SBP) 对氧化应激诱导的皮肤衰老过程的潜在保护机制。我们用 300 µmoL/L 的 H 2 O 2处理人类皮肤成纤维细胞 (HSF)24 小时,然后是 25、50 和 100 µg/mL SBP 24 小时。结果表明,SBP可以增强超氧化物歧化酶(SOD)和谷胱甘肽(GSH)的活性,有效去除多余的ROS,显着改善皮肤细胞中过量ROS引起的细胞形态和活力的变化。此外,SBP可通过TGF-β1/Smads通路促进衰老HSFs中Col I的合成,并通过调节MMPs/TIMPs系统抑制Col I的降解,从而维持ECM结构的稳定性,从而达到抗衰老的目的。目的。最后我们研究了SBP的迁移能力,结果表明100 µg/mL的SBP最有利于衰老细胞的细胞迁移,为后续的动物实验奠定了基础。
更新日期:2022-09-25
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