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Page 4 of 10 Philips et al. Plast Aesthet Res 2022;9:4 https://dx.doi.org/10.20517/2347-9264.2021.83

Figure 2. Table summarizing the anti-photoaging and anti-photocarcinogenic effects of vitamin D. Green plus sign means upregulation;
Red X denotes inhibition. IL-1: Interleukin-1; TNF-α: tumor necrosis factor-α; IL-8: interleukin-8; TGF-β: transforming growth factor-β;
VEGF: vascular endothelial growth factor; MMP: matrix metalloproteinases; 8-OHdG: 8-hydroxy-2’-deoxyguanine; ECM: extracellular
matrix.

these results showed that VD reduced the formation of 8-OHdG and CPDs caused by oxidative stress
through the reduction of ROS in UV-irradiated skin explants, as well as other mutagenic alterations such as
thymine dimers or 8-nitroguanosine .
[43]
INFLAMMATION
Exposure of the skin to UV radiation or environmental pollutants initially causes localized inflammatory
response involving innate immunity, and later adaptive immunity involving the T- and B-lymphocytes [44-48] .
The initial inflammation results in the release of cytokines, such as interleukins (IL) and tumor necrosis
factor (TNF) . These cytokines activate I-κB kinase, which activates the NF-κB transcriptional factor,
[45]
amplifying the expression of inflammatory mediators . The activation of adaptive immunity causes the
[44]
release of Th2 cytokines, such as IL-4, which drives the activation of Janus tyrosine kinases, induces
dimerization of signal transducers of transcription, and increased expression of additional inflammatory
mediators, such as Immunoglobulin E (IgE) [44-48] . IgE antibodies cause the release of histamine and other
inflammatory mediators from basophils and mast cells .
[48]