Cyanidin-3-glucoside inhibits UVB-induced oxidative damage and inflammation by regulating MAP kinase and NF-κB signaling pathways in SKH-1 hairless mice skin.
Cyanidin-3-glucoside inhibits UVB-induced oxidative damage and inflammation by regulating MAP kinase and NF-κB signaling pathways in SKH-1 hairless mice skin.
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DOI：
10.1016/j.taap.2014.06.028
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发表时间：
2014-10-01
影响因子：
3.8
通讯作者：
Shi, Xiang Lin
中科院分区：
文献类型：
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作者：
Pratheeshkumar, Poyil;Son, Young-Ok;Wang, Xin;Divya, Sasidharan Padmaja;Joseph, Binoy;Hitron, John Andrew;Wang, Lei;Kim, Donghern;Yin, Yuanqin;Roy, Ram Vinod;Lu, Jian;Zhang, Zhuo;Wang, Yitao;Shi, Xiang Lin
皮肤癌是美国最常见的癌症之一。暴露于紫外线B（UVB）辐射诱导哺乳动物皮肤炎症和光致癌作用。花青素-3-葡萄糖苷（Cyanidin-3-Glucoside，C3 G）是花青素家族的一员，广泛存在于各种蔬菜和水果中，尤其是可食用浆果中，具有较强的抗氧化和抗癌作用。在这项研究中，我们评估了C3 G对UVB辐射诱导的SKH-1无毛小鼠慢性炎症反应的体内影响，SKH-1无毛小鼠是UVB诱导的皮肤癌发生的良好模型。在这里，我们表明，C3 G抑制UVB诱导的皮肤损伤和炎症SKH-1无毛小鼠。我们的研究结果表明，C3 G抑制谷胱甘肽耗竭，脂质过氧化和骨髓过氧化作用，在小鼠皮肤慢性UVB暴露。C3 G显著降低UVB诱导的与皮肤炎症相关的促炎细胞因子如IL-6和TNF-α的产生。同样，UVB诱导的炎症反应减少C3 G的磷酸化MAP激酶，Erk 1/2，p38，JNK 1/2和MKK 4的水平显着降低。此外，C3 G还降低UVB诱导的环氧合酶-2（考克斯-2）、PGE 2和iNOS水平，这些是众所周知的炎症和癌症的关键介质。C3 G可抑制UVB诱导的NF-κB核转位和IκBα降解。免疫荧光检测显示，局部应用C3 G可抑制慢性UVB暴露小鼠皮肤中8-羟基-2 ′-脱氧鸟苷、增殖细胞核抗原和细胞周期蛋白D1的表达。总之，这些数据表明，C3 G可以提供实质性的保护，对UVB辐射的不利影响，通过调节UVB诱导的MAP激酶和NF-κB信号通路。
Skin cancer is one of the most commonly diagnosed cancers in the United States. Exposure to ultraviolet-B (UVB) radiation induces inflammation and photocarcinogenesis in mammalian skin. Cyanidin-3-Glucoside (C3G), a member of the anthocyanin family, is present in various vegetables and fruits especially in edible berries, and displays potent antioxidant and anticarcinogenic properties. In this study, we have assessed the in vivo effects of C3G on UVB irradiation induced chronic inflammatory responses in SKH-1 hairless mice, a well-established model for UVB-induced skin carcinogenesis. Here, we show that C3G inhibited UVB-induced skin damage and inflammation in SKH-1 hairless mice. Our results indicate that C3G inhibited glutathione depletion, lipid peroxidation and myeloperoxidation in mouse skin by chronic UVB exposure. C3G significantly decreased the production of UVB-induced pro-inflammatory cytokines, such as IL-6 and TNF-α, associated with cutaneous inflammation. Likewise, UVB-induced inflammatory responses were diminished by C3G as observed by a remarkable reduction in the levels of phosphorylated MAP Kinases, Erk1/2, p38, JNK1/2 and MKK4. Furthermore, C3G also decreased UVB-induced cyclooxygenase-2 (COX-2), PGE2 and iNOS levels, which are well-known key mediators of inflammation and cancer. Treatment with C3G inhibited UVB-induced nuclear translocation of NF-κB and degradation of IκBα in mice skin. Immunofluorescence assay revealed that topical application of C3G inhibited the expression of 8-hydroxy-2′-deoxyguanosine, proliferating cell nuclear antigen, and cyclin D1 in chronic UVB exposed mouse skin. Collectively, these data indicates that C3G can provide substantial protection against the adverse effects of UVB radiation by modulating UVB-induced MAP kinase and NF-κB signaling pathways.
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影响因子：
4.7
作者：
Burns, Erin M.;Tober, Kathleen L.;Oberyszyn, Tatiana M.
通讯作者：
Oberyszyn, Tatiana M.
DOI：
10.1159/000064535
发表时间：
2002-09-01
期刊：
SKIN PHARMACOLOGY AND APPLIED SKIN PHYSIOLOGY
影响因子：
--
作者：
de Gruijl, FR
通讯作者：
de Gruijl, FR
影响因子：
2.9
作者：
Fazekas, Z;Gao, DY;Wei, HC
通讯作者：
Wei, HC
影响因子：
3.3
作者：
Khan N;Syed DN;Pal HC;Mukhtar H;Afaq F
通讯作者：
Afaq F
影响因子：
2.7
作者：
Choi, Yeon Ja;Uehara, Yohei;Chung, Hae Young
通讯作者：
Chung, Hae Young