Abstract
Ultraviolet B (UVB) radiation is one of the major predisposing risk factors of skin cancer. The anticancer and photoprotective effects of unoxidized rooibos (Aspalathus linearis) and honeybush (Cyclopia) herbal teas, containing high levels of dihydrochalones and xanthones, respectively, have been demonstrated in skin cancer models in vivo. In the current study, the anti-inflammatory effects of methanol and aqueous extracts of these herbal teas were investigated in a UVB/HaCaT keratinocyte model with intracellular interleukin-1α (icIL-1α) accumulation as a biomarker. Extracts of green tea (Camellia sinensis) served as benchmark. Both extracts of green tea and rooibos, as well as the aqueous extract of C. intermedia, enhanced UVB-induced inhibition of cell viability, proliferation and induction of apoptosis, facilitating the removal of icIL-1α. The underlying mechanisms may involve mitochondrial dysfunction exhibiting pro-oxidant responses via polyphenol-iron interactions. The methanol extracts of honeybush, however, protected against UVB-induced reduction of cell growth parameters, presumably via antioxidant mechanisms that prevented the removal of highly inflamed icIL-1α-containing keratinocytes via apoptosis. The dual antioxidant and/or pro-oxidant role of the polyphenolic herbal tea constituents should be considered in developing preventive strategies against UVB-induced skin carcinogenesis. The indirect removal of UVB damaged keratinocytes by herbal tea extracts via apoptosis may find application in the prevention of photo-induced inflammation.
Highlights
Ultraviolet B (UVB) radiation (280–315 nm) is regarded as one of the major predisposing risk factors of skin cancer as it is known to induce DNA damage, oxidative stress, inflammation and cell cycle dysregulation, pathological events that can lead to malignant transformation in cells [1,2,3].Molecules 2016, 21, 1323; doi:10.3390/molecules21101323 www.mdpi.com/journal/moleculesKeratinocytes are the primary targets of UVB-induced toxic effects [4,5], as a result the most commonly occurring skin cancers develop in the epidermal layer through a multistage process involving initiation, promotion and progression [6,7,8]
UVB activates the production of various pro-inflammatory mediators including the primary (TNF-α and interleukin-1 (IL-1α and β)) and secondary (IL-6, IL-8, IL-10 and IL-4) cytokines that mediate inflammation and immunosuppresion [9,12]
The methanol extract of green tea was more active than its aqueous extract both in the absence and presence of UVB irradiation
Summary
Ultraviolet B (UVB) radiation (280–315 nm) is regarded as one of the major predisposing risk factors of skin cancer as it is known to induce DNA damage, oxidative stress, inflammation and cell cycle dysregulation, pathological events that can lead to malignant transformation in cells [1,2,3].Molecules 2016, 21, 1323; doi:10.3390/molecules21101323 www.mdpi.com/journal/moleculesKeratinocytes are the primary targets of UVB-induced toxic effects [4,5], as a result the most commonly occurring skin cancers develop in the epidermal layer through a multistage process involving initiation, promotion and progression [6,7,8]. UVB activates the production of various pro-inflammatory mediators including the primary A key signalling molecule responsible for the early inflammatory events in skin is IL-1α, a primary cytokine that is constitutively produced in keratinocytes as a biologically active precursor molecule that remains in the cytosol [13,14,15]. Upon cell activation by inflammatory stimuli, cytosolic IL-1α translocates to the nucleus where it activates the production of pro-inflammatory cytokines and growth factors that are involved in the recruitment of immune cells producing reactive oxygen species (ROS) and cell proliferation [16,17]
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