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人参皂苷 Rg1 通过端粒机制保护人成纤维细胞免受补骨脂素和 UVA 诱导的过早衰老。

Ginsenoside Rg1 protects human fibroblasts against psoralen- and UVA-induced premature senescence through a telomeric mechanism.

机构信息

Department of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.

出版信息

Arch Dermatol Res. 2012 Apr;304(3):223-8. doi: 10.1007/s00403-012-1221-9. Epub 2012 Feb 15.

DOI:10.1007/s00403-012-1221-9
PMID:22350182
Abstract

This study was aimed to investigate the protective effects of ginsenoside Rg1 on 8-methoxypsoralen(8-MOP)/Ultraviolet A (UVA)-induced premature senescence in human fibroblasts, and the underlying mechanism. We established a stress-induced premature senescence model by 8-MOP/UVA irradiation. The aging condition was determined by histochemical staining of senescence-associated β-galactosidase (SA-β-gal). Relative telomere length was calculated by the ratio of the amount of telomere DNA versus single copy DNA by real-time polymerase chain reaction, and protein levels of p-P53, p21(WAF-1) and p16(INK-4a) were estimated by Western blotting. Compared with the 8-MOP/UVA treatment group, we found that the irradiated fibroblasts pretreated with ginsenoside Rg1 demonstrated a decrease in the expression of SA-β-gal, a downregulation in the level of senescence-associated proteins, and a deceleration in telomere shortening. Taken together, these results suggest that ginsenoside Rg1 significantly antagonizes premature senescence induced by 8-MOP/UVA in fibroblasts.

摘要

本研究旨在探讨人参皂苷 Rg1 对 8-甲氧基补骨脂素(8-MOP)/长波紫外线(UVA)诱导的人成纤维细胞过早衰老的保护作用及其机制。我们通过 8-MOP/UVA 照射建立了应激诱导的过早衰老模型。衰老状态通过衰老相关β-半乳糖苷酶(SA-β-gal)的组织化学染色来确定。通过实时聚合酶链反应计算端粒 DNA 与单拷贝 DNA 的比值来计算相对端粒长度,并用 Western blot 法测定 p-P53、p21(WAF-1)和 p16(INK-4a)的蛋白水平。与 8-MOP/UVA 处理组相比,我们发现经人参皂苷 Rg1 预处理的辐照成纤维细胞中 SA-β-gal 的表达减少,衰老相关蛋白水平下调,端粒缩短速度减慢。综上所述,这些结果表明人参皂苷 Rg1 能显著拮抗 8-MOP/UVA 诱导的成纤维细胞过早衰老。

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