Kimura Yoshiyuki, Sumiyoshi Maho, Taniguchi Masahiko
Department of Natural Product Sciences, Faculty of Pharmaceutical Sciences, Osaka Medical and Pharmaceutical University, Nasahara, Takatsuki City, Osaka, 569-1094, Japan.
Division of Biochemical Pharmacology, Department of Functional Biomedicine, Ehime University Graduate School of Medicine, Toon City, Ehime, 791-0295, Japan.
Photochem Photobiol Sci. 2025 Mar;24(3):479-497. doi: 10.1007/s43630-025-00700-3. Epub 2025 Mar 17.
Non-melanoma skin cancer accounted for over one million new cases, according to the Global Cancer Statistics 2020 report. Moreover, UV radiation causes photodamage (skin inflammation and angiogenesis), photoaging (increases in skin wrinkle and reduction in skin elasticity). This study investigated the preventive effects of baicalein against skin damage, aging, tumorigenesis and tumor growth in long-term UVB irradiated hairless mice. Five-week-old male mice were divided into the following groups: a non-UVB group (control), vehicle-treated UVB group (UVB control), and UVB groups treated with two different doses of baicalein (10 and 30 mg/kg, twice daily). The mice were exposed to UVB irradiation (36-192 mJ/cm) three times per week for 23 weeks. Baicalein was orally administered at the specified doses for the same duration. Skin cytokine, chemokine, and vascular endothelial growth factor (VEGF) levels were measured using ELISA kits. Baicalein (at doses of 10 and 30 mg/kg) suppressed UVB-induced increases in skin thickness, improved skin elasticity, and reduced the number and growth of skin tumors. Additionally, baicalein inhibited UVB-induced increases in IL-1β, IL-6, MCP-1, MIF, VEGF, p53, COX-2, total/phospho-NF-κB expression levels in the skin. Immunohistochemical analysis revealed that baicalein attenuated UVB-induced increases in the number of Ki-67-, and HIF-1α-positive cells. The preventive effects of baicalein on skin damage and skin tumor growth in chronically UVB-irradiated mice were associated with reduced skin cytokine levels through the down-regulation of COX-2, phosphorylated NF-κB p65, and HIF-1α expression.
根据《2020年全球癌症统计报告》，非黑色素瘤皮肤癌新增病例超过100万例。此外，紫外线辐射会导致光损伤（皮肤炎症和血管生成）、光老化（皮肤皱纹增加和皮肤弹性降低）。本研究调查了黄芩苷对长期紫外线B照射的无毛小鼠皮肤损伤、衰老、肿瘤发生和肿瘤生长的预防作用。将5周龄雄性小鼠分为以下几组：非紫外线B组（对照组）、赋形剂处理的紫外线B组（紫外线B对照组）以及用两种不同剂量黄芩苷（10和30mg/kg，每日两次）处理的紫外线B组。小鼠每周接受3次紫外线B照射（36 - 192mJ/cm），持续23周。黄芩苷按指定剂量口服相同时间。使用酶联免疫吸附测定试剂盒测量皮肤细胞因子、趋化因子和血管内皮生长因子（VEGF）水平。黄芩苷（10和30mg/kg剂量）抑制了紫外线B诱导的皮肤厚度增加，改善了皮肤弹性，并减少了皮肤肿瘤的数量和生长。此外，黄芩苷抑制了紫外线B诱导的皮肤中IL - 1β、IL - 6、MCP - 1、MIF、VEGF、p53、COX - 2、总/磷酸化NF - κB表达水平的增加。免疫组织化学分析显示，黄芩苷减弱了紫外线B诱导的Ki - 67和HIF - 1α阳性细胞数量的增加。黄芩苷对长期紫外线B照射小鼠皮肤损伤和皮肤肿瘤生长的预防作用与通过下调COX - 2、磷酸化NF - κB p65和HIF - 1α表达而降低皮肤细胞因子水平有关。
