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黄芪甲苷对人成纤维细胞紫外线A诱导光老化的保护作用。

Protective effects of astragaloside against ultraviolet A-induced photoaging in human fibroblasts.

作者信息

Liu Xin, Min Wei

机构信息

Department of Dermatology, Jiangsu Province Official Hospital, Nanjing 210024, Jiangsu Province, China; E-mail:

出版信息

Zhong Xi Yi Jie He Xue Bao. 2011 Mar;9(3):328-32. doi: 10.3736/jcim20110315.

Abstract

OBJECTIVE

In this study, we aim to investigate the protective effects of astragaloside on ultraviolet A (UVA)-induced photoaging in human fibroblasts and its possible mechanisms.

METHODS

Subconfluent fibroblasts were cultured and divided into normal control group, astragaloside group, UVA irradiation group and UVA plus astragaloside group. The cells were shammed or irradiated with 10 J/cm(2) of UVA irradiation and treated with 20 μg/mL astragaloside. The aging condition was determined by histochemical staining of senescence-associated β-galactosidase (SA-β-gal). Concentration of transforming growth factor-β1 (TGF-β1) in the supernatant was determined by enzyme-linked immunosorbent assay, and mRNA levels of matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) were measured by real-time polymerase chain reaction.

RESULTS

UVA irradiation raised the proportion of SA-β-gal-positive cells in comparison with the normal control group (P<0.05). Astragaloside treatment was shown to decrease the level of SA-β-gal compared with the UVA group. With UVA irradiation, the concentration of TGF-β1 in the supernatant decreased, and astragaloside treatment recovered the content of TGF-β1 compared with the UVA irradiation alone (P<0.05). UVA irradiation also up-regulated the mRNA levels of MMP-1 and TIMP-1 (P<0.05). Astragaloside decreased the mRNA level of MMP-1 compared with the UVA irradiation alone, while the TIMP-1 expression increased (P<0.05).

CONCLUSION

Astragaloside can protect the skin from UVA irradiation. The mechanism involved may be related with TGF secretion and decrease of collagen degradation.

摘要

目的

本研究旨在探讨黄芪甲苷对紫外线A(UVA)诱导的人成纤维细胞光老化的保护作用及其可能机制。

方法

培养接近汇合的成纤维细胞,分为正常对照组、黄芪甲苷组、UVA照射组和UVA+黄芪甲苷组。细胞进行假照射或用10 J/cm²的UVA照射,并给予20 μg/mL黄芪甲苷处理。通过衰老相关β-半乳糖苷酶(SA-β-gal)组织化学染色确定衰老状况。采用酶联免疫吸附测定法测定上清液中转化生长因子-β1(TGF-β1)的浓度,通过实时聚合酶链反应检测基质金属蛋白酶-1(MMP-1)和金属蛋白酶组织抑制剂-1(TIMP-1)的mRNA水平。

结果

与正常对照组相比,UVA照射使SA-β-gal阳性细胞比例升高(P<0.05)。与UVA组相比,黄芪甲苷处理可降低SA-β-gal水平。UVA照射后,上清液中TGF-β1浓度降低,与单纯UVA照射相比,黄芪甲苷处理可使TGF-β1含量恢复(P<)

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