Diallyl sulfide protects against ultraviolet B-induced skin cancers in SKH-1 hairless mouse: analysis of early molecular events in carcinogenesis.
Cherng JM, Tsai KD, Perng DS, Wang JS, Wei CC, Lin JC.
Source
Department of Internal Medicine, Chung Shan Medical University Hospital, Chung Shan Medical University, Taichung, Taiwan, ROC Department of Internal Medicine, China Medical University and Beigang Hospital, Yunlin, Taiwan, ROC Institute of Molecular Biology, National Chung Cheng University, Chiayi, Taiwan, ROC Department of Internal Medicine, E-Da Hospital, I-Shou University, Kaohsiung, Taiwan, ROC Department of Internal Medicine, Antai Tian-Sheng Memorial Hospital, Pingtung, Taiwan, ROC Department of Internal Medicine, Taipei Medical University, Taipei, Taiwan, ROC Cellular Virology Unit, Centers for Disease Control and Prevention, Division of Viral Hepatitis, Atlanta, GA, USA.
Abstract
Background: Diallyl sulfide (DAS) has been shown to have a preventive effect against various cancers. Aims and objectives: We evaluated the protective effects of DAS in regression of ultraviolet B (UVB)-induced skin tumor formation in SKH-1 hairless mice and its underlying early molecular biomarkers. Methods: We examined the efficacy of DAS in UVB light-induced skin lesion in SKH-1 hairless mice and the associated molecular events. Results: Mice irradiated with UVB at 180 mJ/cm(2) twice per week elicited 100% tumor incidence at 20 weeks. The topical application of DAS before UVB irradiation caused a delay in tumor appearance, multiplicity, and size. The topical application of DAS before and immediately after a single UVB irradiation (180 mJ/cm(2) ) resulted in a significant decrease in UVB-induced thymine dimer-positive cells, expression of proliferative cell nuclear antigen (PCNA), terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, and apoptotic sunburn cells, together with an increase in p53 and p21/Cip1-positive cell population in the epidermis. Simultaneously, DAS also significantly inhibited nuclear factor-κB (NF-κB), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and nitric oxide (NO) levels. Conclusions: The protective effect of DAS against photocarcinogenesis is accompanied by the down-regulation of cell-proliferative controls, involving thymine dimer, PCNA, apoptosis, transcription factors NF-κB, and of inflammatory responses involving COX-2, PGE2, and NO, and up-regulation of p53, p21/Cip1 to prevent DNA damage and facilitate DNA repair.
© 2011 John Wiley & Sons A/S.
PMID:21535167[PubMed - as supplied by publisher]
Diallyl sulfide protects against ultraviolet B-ind... [Photodermatol Photoimmunol Photomed. 2011] - PubMed result
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