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姜黄素通过 hsa-miR-4535 介导的 TGFβ/Smad 信号通路对 HO/UVB 诱导的皮肤成纤维细胞胶原降解的保护作用。

Protective effects of galangin against HO/UVB-induced dermal fibroblast collagen degradation via hsa-microRNA-4535-mediated TGFβ/Smad signaling.

机构信息

Department of Plastic and Reconstructive Surgery, China Medical University Hospital, Taichung 40447, Taiwan, ROC.

School of Medicine, China Medical University, Taichung 40447, Taiwan, ROC.

出版信息

Aging (Albany NY). 2021 Dec 10;13(23):25342-25364. doi: 10.18632/aging.203750.

DOI:10.18632/aging.203750
PMID:34890367
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8714160/
Abstract

This study aimed to investigate the mechanism underlying the protective effects of galangin against HO/UVB-induced damage using and models of photodamage. Moreover, we identified the involvement of miRNA regulation in this process. The HO/UVB-treated HS68 human dermal fibroblasts and UVB-induced C57BL/6J nude mice were used as and models of photodamage. The results showed that galangin treatment alleviated HO/UVB-induced reduction in cell viability, TGFβ/Smad signaling impairment, and dermal aging. Based on the results of microRNA array analyses and database searches, hsa-miR-4535 was identified as a potential candidate miRNA that targets Smad4. , galangin treatment activated Smad2/3/4 complex and inhibited hsa-miR-4535 expression in H2O2/UVB-exposed cells. , topical application of low (12 mg/kg) and high doses (24 mg/kg) of galangin to the dorsal skin of C57BL/6J nude mice significantly alleviated UVB-induced skin photodamage by promoting TGFβ/Smad collagen synthesis signaling, reducing epidermal hyperplasia, wrinkle formation, and skin senescence, as well as inhibiting hsa-miR-4535 expression. Taken together, our findings indicate a link between hsa-miR-4535 and TGFβ/Smad collagen synthesis signaling and suggest these factors to be involved in the photo-protective mechanism of galangin in dermal fibroblasts against HO/UVB-induced aging. The evidence indicated that galangin with anti-aging properties can be considered as a supplement in skin care products.

摘要

本研究旨在探讨滨蒿素对 HO/UVB 诱导损伤的保护作用机制，采用 和 光损伤模型进行研究。此外，我们还确定了 miRNA 调控在此过程中的参与。HO/UVB 处理的 HS68 人真皮成纤维细胞和 UVB 诱导的 C57BL/6J 裸鼠分别作为 和 光损伤模型。结果表明，滨蒿素治疗可减轻 HO/UVB 诱导的细胞活力降低、TGFβ/Smad 信号受损和皮肤衰老。基于 microRNA 阵列分析和数据库搜索的结果，hsa-miR-4535 被鉴定为潜在的候选 miRNA，靶向 Smad4。 ，滨蒿素治疗可激活 H2O2/UVB 暴露细胞中的 Smad2/3/4 复合物并抑制 hsa-miR-4535 的表达。 ，低（12 mg/kg）和高剂量（24 mg/kg）的滨蒿素局部应用于 C57BL/6J 裸鼠背部皮肤可显著减轻 UVB 诱导的皮肤光损伤，通过促进 TGFβ/Smad 胶原合成信号，减少表皮过度增生、皱纹形成和皮肤衰老，同时抑制 hsa-miR-4535 的表达。综上所述，我们的研究结果表明 hsa-miR-4535 与 TGFβ/Smad 胶原合成信号之间存在联系，并表明这些因素可能参与了滨蒿素在真皮成纤维细胞中对抗 HO/UVB 诱导衰老的光保护机制。该研究结果表明，具有抗衰老特性的滨蒿素可以被视为护肤品中的一种补充成分。

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