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超氧化物歧化酶1抑制小鼠皮肤中α-黑素细胞刺激素和紫外线B诱导的黑素生成。

Superoxide dismutase 1 inhibits alpha-melanocyte stimulating hormone and ultraviolet B-induced melanogenesis in murine skin.

作者信息

Oh Chang Taek, Lee Dohyun, Koo Kyotan, Lee Jay, Yoon Ho Sang, Choi Yoo Mi, Kwon Tae-Rin, Kim Beom Joon

机构信息

Department of Dermatology, Chung-Ang University College of Medicine, Seoul, Korea. ; Department of Medicine, Graduate School, Chung-Ang University, Seoul, Korea.

Nutrex Technology R&D Center, Seoul, Korea.

出版信息

Ann Dermatol. 2014 Dec;26(6):681-7. doi: 10.5021/ad.2014.26.6.681. Epub 2014 Nov 26.

Abstract

BACKGROUND

Over the last decade, the incidence of ultraviolet B (UVB)-related skin problems has increased. Oxidative stress caused by UVB induces the secretion of melanocyte growth and activating factors from keratinocytes, which results in the formation of cutaneous hyperpigmentation. Therefore, increasing the antioxidant abilities of skin cells is thought to be a beneficial strategy for the development of sunscreen agents. Superoxide dismutase 1 (SOD1) is an antioxidant enzyme that is known to exhibit antioxidant properties.

OBJECTIVE

The purpose of this study was to investigate the effect of SOD1 on alpha-melanocyte stimulating hormone (α-MSH) and UVB-induced melanogenesis in B16F10 melanoma cells and HRM-2 melanin-possessing hairless mice.

METHODS

The inhibitory effect of SOD1 on tyrosinase activity was evaluated in a cell-free system. Additional experiments were performed using B16F10 melanoma cells to demonstrate the effects of SOD1 in vitro, and HRM-2 melanin-possessing hairless mice were used to evaluate the antimelanogenic effects of SOD1 in vivo.

RESULTS

We found that SOD1 inhibited melanin production in a dose-dependent manner without causing cytotoxicity in B16F10 melanoma cells. SOD1 did not inhibit tyrosinase activity under cell-free conditions. The results indicate that SOD1 may reduce pigmentation by an indirect, nonenzymatic mechanism. We also found that SOD1 decreased UVB-induced melanogenesis in HRM-2 melanin-possessing hairless mice, as visualized through hematoxylin and eosin staining and Fontana-Masson staining.

CONCLUSION

Our results indicate that SOD1 has an inhibitory effect on α-MSH and UVB-induced melanogenesis, indicating that SOD1 may be a promising sunscreen agent.

摘要

背景

在过去十年中,与紫外线B(UVB)相关的皮肤问题发病率有所上升。UVB引起的氧化应激诱导角质形成细胞分泌黑素细胞生长和激活因子,从而导致皮肤色素沉着的形成。因此,提高皮肤细胞的抗氧化能力被认为是开发防晒剂的有益策略。超氧化物歧化酶1(SOD1)是一种已知具有抗氧化特性的抗氧化酶。

目的

本研究旨在探讨SOD1对B16F10黑色素瘤细胞和HRM-2有黑色素的无毛小鼠中α-黑素细胞刺激素(α-MSH)和UVB诱导的黑色素生成的影响。

方法

在无细胞系统中评估SOD1对酪氨酸酶活性的抑制作用。使用B16F10黑色素瘤细胞进行额外实验以证明SOD1在体外的作用,并使用HRM-2有黑色素的无毛小鼠评估SOD1在体内的抗黑色素生成作用。

结果

我们发现SOD1以剂量依赖性方式抑制B16F10黑色素瘤细胞中的黑色素生成,且不引起细胞毒性。在无细胞条件下,SOD1不抑制酪氨酸酶活性。结果表明SOD1可能通过间接的非酶机制减少色素沉着。我们还发现,通过苏木精和伊红染色以及Fontana-Masson染色可见,SOD1可减少HRM-2有黑色素的无毛小鼠中UVB诱导的黑色素生成。

结论

我们的结果表明SOD1对α-MSH和UVB诱导的黑色素生成具有抑制作用,表明SOD1可能是一种有前景的防晒剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa5b/4252663/78ff51cea11a/ad-26-681-g001.jpg

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