In this study, the effect of
caffeic acid (CA) on both acute and chronic UVB-irradiation-induced
inflammation and photocarcinogenesis was investigated in Swiss albino mice. Animals were exposed to 180 mJ cm(-2) of UVB once daily for 10 consecutive days and thrice weekly for 30 weeks for acute and chronic study respectively. UVB exposure for 10 consecutive days showed
edema formation, increased lipid peroxidation and decreased
antioxidant status with activation of inflammatory molecules such as TNF-α,
IL-6, COX-2 and NF-κB. However, CA (15 mg per kg.b.wt.) administration before each UVB exposure decreased lipid peroxidation, inflammatory markers expression and enhanced
antioxidant status probably through the activation of
peroxisome proliferator-activated receptors (PPARγ) in the mice skin. PPARγ is considered a potential target for photochemoprevention because it inhibits UVB-mediated inflammatory responses. In this study, UVB exposure for 30 weeks caused
squamous cell carcinoma and upregulation of iNOS,
VEGF and TGF-β and downregulation of p53 and
tumor incidence in the mice skin. Both topical (CAT) and intraperitoneal (CAIP) treatment before each UVB exposure downregulates iNOS,
VEGF, TGF-β, upregulates p53 and reduces
tumors multiplicity in the mice skin. Thus, CA offers protection against UVB-induced photocarcinogenesis probably through activation of anti-inflammatory
transcription factor PPARγ in the mice.