Protection against Ultraviolet A-Induced Skin Apoptosis and Carcinogenesis through the Oxidative Stress Reduction Effects of N -(4-bromophenethyl) Caffeamide, A Propolis Derivative

• Published in: Antioxidants 2020-04, Vol.9 (4), p.335
• Main Authors: Kuo, Yueh-Hsiung, Chiang, Hung-Lung, Wu, Po-Yuan, Chu, Yin, Chang, Qiao-Xin, Wen, Kuo-Ching, Lin, Chien-Yih, Chiang, Hsiu-Mei
• Format: Article
• Language: English
• Subjects: Aging; Antioxidants; Apoptosis; B-cell lymphoma; BAX protein; c-Fos protein; c-Jun protein; Carcinogenesis; Caspase-3; Cell culture; Cyclooxygenase-2; Deoxyribonucleic acid; DNA; DNA damage; Enzyme-linked immunosorbent assay; Fibroblasts; Free radicals; Gelatinase A; Genotoxicity; Health aspects; Heme; Heme oxygenase (decyclizing); Inflammation; Interleukin 6; JNK protein; Keratinocytes; Kinases; Lymphocytes B; Matrix metalloproteinase; Metalloproteinase; N-(4-bromophenethyl) caffeamide; Nitric oxide; Oxidation; Oxidative stress; Proteins; Reactive oxygen species; Skin; Transcription factors; Tumor necrosis factor-TNF; Ultraviolet radiation; Western blotting
• ISSN: 2076-3921; 2076-3921
• DOI: 10.3390/antiox9040335

Ultraviolet A (UVA) is a major factor in skin aging and damage. Antioxidative materials may ameliorate this UV damage. This study investigated the protective properties of N-(4-bromophenethyl) caffeamide (K36H) against UVA-induced skin inflammation, apoptosis and genotoxicity in keratinocytes. The protein expression or biofactor concentration related to UVA-induced skin damage were identified using an enzyme-linked immunosorbent assay and western blotting. K36H reduced UVA-induced intracellular reactive oxygen species generation and increased nuclear factor erythroid 2-related factor 2 translocation into the nucleus to upregulate the expression of heme oxygenase-1, an intrinsic antioxidant enzyme. K36H inhibited UVA-induced activation of extracellular-signal-regulated kinases and c-Jun N-terminal kinases, reduced the overexpression of matrix metalloproteinase (MMP)-1 and MMP-2 and elevated the expression of the metalloproteinase-1 tissue inhibitor. Moreover, K36H inhibited the phosphorylation of c-Jun and downregulated -Fos expression. K36H attenuated UVA-induced Bax and caspase-3 expression and upregulated antiapoptotic protein B-cell lymphoma 2 expression. K36H reduced UVA-induced DNA damage. K36H also downregulated inducible nitric oxide synthase, cyclooxygenase-2 and interleukin-6 expression as well as the subsequent generation of prostaglandin E and nitric oxide. We observed that K36H ameliorated UVA-induced oxidative stress, inflammation, apoptosis and antiphotocarcinogenic activity. K36H can potentially be used for the development of antiphotodamage and antiphotocarcinogenic products.