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窄谱中波紫外线对人皮肤成纤维细胞中基质金属蛋白酶-1、转化生长因子-β1及I型胶原蛋白表达的影响

The effect of narrowband ultraviolet B on the expression of matrix metalloproteinase-1, transforming growth factor-beta1 and type I collagen in human skin fibroblasts.

作者信息

Choi C P, Kim Y I, Lee J W, Lee M H

机构信息

Department of Dermatology, College of Medicine, Kyunghee University, Seoul, Korea.

出版信息

Clin Exp Dermatol. 2007 Mar;32(2):180-5. doi: 10.1111/j.1365-2230.2006.02309.x. Epub 2006 Nov 27.

Abstract

BACKGROUND

Ultraviolet (UV) irradiation induces chronic skin diseases, such as skin cancer and photoageing, and the mechanisms of this skin damage are associated with the upregulation of matrix metalloproteinases (MMPs) and decreased collagen synthesis. Narrowband ultraviolet B (NB-UVB) radiation is a relatively new treatment modality for vitiligo and psoriasis. However, the mechanism of NB-UVB action on photoageing is not completely understood. Aims. We investigated the effects of NB-UVB on the expression of MMP-1, transforming growth factor (TGF)-beta1 and type I collagen in cultured human skin fibroblasts.

METHODS

Cultured human fibroblasts were irradiated with either NB-UVB (50-800 mJ/cm(2)) or broadband UVB (BB-UVB; 25 mJ/cm(2)). The expression of MMP-1, TGF-beta1 and type I collagen mRNA was determined by reverse-transcription PCR. Expression of MMP-1 and TGF-beta1 protein was determined by ELISA and that of type I collagen by Western blotting.

RESULTS

NB-UVB induced the expression of MMP-1 and reduced the expression of TGF-beta1 and type I collagen at the mRNA and protein levels in a dose-dependent manner. The expression of type I collagen protein decreased more after irradiation with 25 mJ/cm(2) of BB-UVB than 400 mJ/cm(2) of NB-UVB.

CONCLUSIONS

This study indicates that NB-UVB irradiation reduces type I collagen synthesis in human skin fibroblasts by inhibiting TGF-beta1 expression and stimulating the release of MMP-1. It also suggested that the photoageing-related effects of NB-UVB are weaker than those of BB-UVB in vitro.

摘要

背景

紫外线(UV)照射可诱发慢性皮肤疾病,如皮肤癌和光老化,这种皮肤损伤的机制与基质金属蛋白酶(MMPs)的上调及胶原蛋白合成减少有关。窄谱中波紫外线(NB-UVB)辐射是治疗白癜风和银屑病的一种相对较新的方法。然而,NB-UVB对光老化作用的机制尚未完全明确。目的:我们研究了NB-UVB对培养的人皮肤成纤维细胞中MMP-1、转化生长因子(TGF)-β1和I型胶原蛋白表达的影响。

方法

用NB-UVB(50 - 800 mJ/cm²)或宽带UVB(BB-UVB;25 mJ/cm²)照射培养的人成纤维细胞。通过逆转录PCR测定MMP-1、TGF-β1和I型胶原蛋白mRNA的表达。通过酶联免疫吸附测定法(ELISA)测定MMP-1和TGF-β1蛋白的表达,通过蛋白质免疫印迹法测定I型胶原蛋白的表达。

结果

NB-UVB以剂量依赖性方式在mRNA和蛋白质水平诱导MMP-1的表达,并降低TGF-β1和I型胶原蛋白的表达。与400 mJ/cm²的NB-UVB照射相比,25 mJ/cm²的BB-UVB照射后I型胶原蛋白蛋白的表达下降得更多。

结论

本研究表明,NB-UVB照射通过抑制TGF-β1表达和刺激MMP-1的释放来减少人皮肤成纤维细胞中I型胶原蛋白的合成。这也表明,在体外,NB-UVB与光老化相关的作用比BB-UVB弱。

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