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没食子酸表没食子儿茶素酯对角质形成细胞系中紫外线 B 诱导的光损伤的影响。

Effect of epigallocatechingallate on ultraviolet B-induced photo-damage in keratinocyte cell line.

机构信息

Department of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.

出版信息

Am J Chin Med. 2006;34(5):911-22. doi: 10.1142/S0192415X06004387.

Abstract

One type of traditional Chinese medicines, epigallocatechingallate (EGCG) has been commonly used as a clinical and skin health protective ingredient. It has been known to have photo-protective, anti-inflammatory, and anti-oxidant effects. However, little is known about the mechanisms of EGCG on UV-induced photo-aging and photo-carcinogenesis. In the present study, we investigated the photo-protective mechanisms of EGCG on UVB-induced skin damage, including the potency of EGCG to inhibit the UVB-induced cytotoxicity, secretion of cytokine (IL-6 and TNF-alpha), cellular apoptosis, expression of apoptosis-regulatory genes (p53-p21) and c-fos gene in cultured immortalized human keratinocyte HaCaT cells. EGCG treatment decreased UVB- induced cell cytotoxicity and apoptosis. It also inhibited the mRNA expressions of apoptosis-regulatory gene (p53 and p21) and c-fos gene. These results suggest that EGCG may have an inhibitory effect on UVB-induced photo-damage and apoptosis by blocking the cytokine secretion and the mRNA expressions of p53, p21 and c-fos genes.

摘要

一种传统中药,表没食子儿茶素没食子酸酯(EGCG)已被广泛用作临床和皮肤保健的成分。它具有光保护、抗炎和抗氧化作用。然而,关于 EGCG 对 UV 诱导的光老化和光致癌作用的机制知之甚少。在本研究中,我们研究了 EGCG 对 UVB 诱导皮肤损伤的光保护机制,包括 EGCG 抑制 UVB 诱导的细胞毒性、细胞因子(IL-6 和 TNF-α)分泌、细胞凋亡、凋亡调节基因(p53-p21)和 c-fos 基因表达的能力在培养的永生化人角质形成细胞 HaCaT 细胞中。EGCG 处理可降低 UVB 诱导的细胞毒性和细胞凋亡。它还抑制了凋亡调节基因(p53 和 p21)和 c-fos 基因的 mRNA 表达。这些结果表明,EGCG 可能通过阻断细胞因子分泌和 p53、p21 和 c-fos 基因的 mRNA 表达,对 UVB 诱导的光损伤和细胞凋亡具有抑制作用。

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