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去甲乌药碱(一种来自[具体来源未给出]的强效化合物)对紫外线B诱导的无毛小鼠光老化的影响。

Effects of the Higenamine, a Potent Compound from , on UVB-Induced Photoaging in Hairless Mice.

作者信息

Lim Hye-Sun, Jang Yumi, Park Gunhyuk

机构信息

Herbal Medicine Resources Research Center, Korea Institute of Oriental Medicine, 111 Geonjae-ro, Naju-si, Jeollanam-do 58245, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2022 Apr 27;2022:9116642. doi: 10.1155/2022/9116642. eCollection 2022.

DOI:10.1155/2022/9116642
PMID:35529934
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9068300/
Abstract

AIM

Higenamine [1-[(4-hydroxyphenyl) methyl]-1, 2, 3, 4-tetrahydroisoquinoline-6, 7-diol], a potent cardiotonic compound from , contributes to vascular relaxation and bronchodilation. However, the effects and mechanisms of action of higenamine on skin aging remain poorly understood. In this study, the effects of higenamine on UVB-induced photoaging were examined in the hairless mouse model.

METHODS

The dorsal skin of hairless mice (CrlOri : SKH1) was exposed to chronic UVB irradiation (100-300 mJ/cm for 6 weeks), with subsequent administration of higenamine (1-20 mg/kg, p.o.) for 2 weeks. TGF-, Smad3 DNA-binding phosphorylation, and COL1A1 levels were analyzed by immunohistochemistry, and histological analysis of the skin was performed via H&E and MT staining.

RESULTS

Higenamine increased TGF-, Smad3 DNA-binding phosphorylation, and COL1A1 expression in primary human fibroblast cells and mouse skin. Higenamine suppressed UVB-induced photoaging via skin recovery, improved epidermal thickness, and prevented Smad3, DNA-binding phosphorylation, and COL1A1 depletion via TGF- signaling.

CONCLUSION

Higenamine enhances collagen production in the skin through TGF-/Smad3 signaling and potentially suppresses UVB-induced skin aging.

摘要

目的

去甲乌药碱[1-[(4-羟基苯基)甲基]-1,2,3,4-四氢异喹啉-6,7-二醇]是一种从[来源未提及]中提取的强效强心化合物,具有血管舒张和支气管扩张作用。然而,去甲乌药碱对皮肤衰老的影响及其作用机制仍知之甚少。在本研究中,我们在无毛小鼠模型中研究了去甲乌药碱对紫外线B(UVB)诱导的光老化的影响。

方法

将无毛小鼠(CrlOri : SKH1)背部皮肤暴露于慢性UVB照射(100 - 300 mJ/cm²,持续6周),随后给予去甲乌药碱(1 - 20 mg/kg,口服)2周。通过免疫组织化学分析转化生长因子(TGF)-β、Smad3 DNA结合磷酸化和Ⅰ型胶原蛋白α1(COL1A1)水平,并通过苏木精和伊红(H&E)染色及甲苯胺蓝(MT)染色对皮肤进行组织学分析。

结果

去甲乌药碱可增加原代人成纤维细胞和小鼠皮肤中TGF-β、Smad3 DNA结合磷酸化及COL1A1的表达。去甲乌药碱通过促进皮肤恢复抑制UVB诱导的光老化,改善表皮厚度,并通过TGF-β信号通路防止Smad3、DNA结合磷酸化及COL1A1的减少。

结论

去甲乌药碱通过TGF-β/Smad3信号通路增强皮肤中的胶原蛋白生成,并可能抑制UVB诱导的皮肤衰老。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3cb/9068300/b0d9ed4233f3/ECAM2022-9116642.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3cb/9068300/522879747e7d/ECAM2022-9116642.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3cb/9068300/4f1c2f384a9e/ECAM2022-9116642.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3cb/9068300/1c82ade29452/ECAM2022-9116642.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3cb/9068300/82c75cbe1820/ECAM2022-9116642.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3cb/9068300/e77f38222431/ECAM2022-9116642.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3cb/9068300/b0d9ed4233f3/ECAM2022-9116642.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3cb/9068300/522879747e7d/ECAM2022-9116642.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3cb/9068300/4f1c2f384a9e/ECAM2022-9116642.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3cb/9068300/1c82ade29452/ECAM2022-9116642.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3cb/9068300/82c75cbe1820/ECAM2022-9116642.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3cb/9068300/e77f38222431/ECAM2022-9116642.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3cb/9068300/b0d9ed4233f3/ECAM2022-9116642.006.jpg

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