Involvement of nitric oxide in UVB-induced pigmentation in guinea pig skin
Involvement of nitric oxide in UVB-induced pigmentation in guinea pig skin
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DOI：
10.1034/j.1600-0749.2000.130509.x
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发表时间：
2000-10-01
期刊：
影响因子：
--
通讯作者：
Miyachi, Y
中科院分区：
文献类型：
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作者：
Horikoshi, T;Nakahara, M;Miyachi, Y
紫外线(UV)B辐射会导致皮肤出现红斑和延迟的色素沉着，这是已知涉及的各种毒性和调节事件。一氧化氮合酶(NO)是由L精氨酸购买一氧化氮合酶(NOSs)产生的，NO的产生是对UVB刺激的反应，NO的产生在红斑的发生发展中起着重要的作用。近年来，NO在体外被证明是一种刺激黑素细胞的黑素原，然而，目前还没有已知的体内数据支持这一发现。在这项研究中，我们研究了在使用一氧化氮合酶抑制剂的动物模型中，一氧化氮在紫外线诱导的色素沉着中的作用。在紫外线照射前3天开始，每天局部使用一氧化氮合酶抑制剂L(N-硝基L精氨酸甲酯盐酸盐)于豚鼠皮肤，可减少紫外线照射所致的豚鼠皮肤红斑。L每日序贯治疗可明显抑制皮肤延迟色素沉着和多巴酚丁胺阳性黑素细胞数量的增加。此外，用NAME治疗的皮肤在UVB照射后13天的黑色素含量显著低于对照组。相反，L-NAME的无效异构体D-NAME(N-硝基-D-精氨酸甲酯盐酸盐)对紫外线诱导的皮肤反应没有影响。这些结果表明，NO的产生可能参与了UVB诱导的色素沉着的调节。
Ultraviolet (UV) B irradiation evolves erythema and delayed pigmentation in skin, where a variety of toxic and modulating events are known to be involved. Nitric oxide (NO) is generated from L-arginine buy NO synthases (NOS), Production of NO is enhanced in response to UVB-stimulation and has an important role in the development of erythema, NO has recently been demonstrated as a melanogen which stimulates melanocytes in vitro, however, no known in vivo data has been reported to support this finding. In this study, we investigated the contribution of NO with UV-induced pigmentation in an animal model using an NOS inhibitor. UVB-induced erythema in guinea pig skin was reduced when an NOS inhibit or, L-NAME (N-nitro-L-arginine methylester hydrochloride), was topically applied to the skin daily beginning 3 days before UVB-irradiation. Delayed pigmentation and an increased number of DOPA-positive melanocytes in the skin were markedly suppressed by sequential daily treatment with L-NAME. Furthermore, melanin content 13 days after UVB-irradiation was significantly lower in skin treated with NAME than in the controls. In contrast, D-NAME (N-nitro-D-arginine methylester hydrochloride), an ineffective isomer of L-NAME, demonstrated no effect on these UV-induced skin responses. These results suggest that NO production may contribute to the regulation of UVB-induced pigmentation.