Nutraceutical Strategies for Alleviation of UVB Phototoxicity.
Mark F McCartyCarina BenzviAristo VojdaniLerner AaronPublished in: Experimental dermatology (2023)
UVB exposure of keratinocytes promotes carcinogenesis by inducing pyrimidine dimer lesions in DNA, suppressing the nucleotide excision repair mechanism required to fix them, inhibiting the apoptosis required for elimination of initiated cells, and driving cellular proliferation. Certain nutraceuticals - most prominently spirulina, soy isoflavones, long-chain omega-3 fatty acids, the green tea catechin epigallocatechin gallate (EGCG) and Polypodium leucotomos extract - have been shown to oppose photocarcinogenesis, as well as sunburn and photoaging, in UVB-exposed hairless mice. It is proposed that spirulina provides protection in this regard via phycocyanobilin-mediated inhibition of Nox1-dependent NADPH oxidase; that soy isoflavones do so by opposing NF-κB transcriptional activity via estrogen receptor-beta; that the benefit of eicosapentaenoic acid reflects decreased production of prostaglandin E2; and that EGCG counters UVB-mediated phototoxicity via inhibition of the epidermal growth factor receptor. The prospects for practical nutraceutical down-regulation of photocarcinogenesis, sunburn, and photoaging appear favorable.
Keyphrases
- signaling pathway
- epidermal growth factor receptor
- estrogen receptor
- cell cycle arrest
- induced apoptosis
- pi k akt
- oxidative stress
- tyrosine kinase
- fatty acid
- advanced non small cell lung cancer
- cell death
- endoplasmic reticulum stress
- gene expression
- lps induced
- type diabetes
- cell free
- circulating tumor
- adipose tissue
- metabolic syndrome
- inflammatory response
- insulin resistance