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Introduction
Ultraviolet (UV) radiation is a major source of skin damage, where daylight UV is composed of three different types classified by wavelengths: UV-A (320–400 nm), UV-B (290–320 nm) and UV-C (<290 nm) (1–5). Skin inflammation after UV exposure is caused by UV-B since it easily triggers the cross-linking of macromolecules, ring-structures and repeated linear molecules (2,3,5).
UV-induced damage can be measured at the cellular level through the production of reactive oxygen species (ROS), leading to genetic mutations, the suppression of gene expression, and inhibition of peptide repair, resulting in inflammation and possibly leading to skin cancer (2,3,5–9). There are three major pathways of UV-induced skin inflammation. The first pathway involves the COX-2 mechanism whereby UV-B exposure induces arachidonic acid release from the phospholipid membrane and the COX-2 enzyme converts it to prostaglandins and free radical molecules (10–13). It has been reported that COX-2 and prostaglandin E2 elevations may be responsible for inflammation and tumorigenesis (11,13,14). The second includes the mitogen-activated protein kinase (MAPK) signaling pathways. After exposure to UV-B, phosphorylation of threonine and tyrosine leads to the activation of the MAPK protein kinase family. SPK/JNK and p38 kinase are activated (phospho-SPK/JNK and phospho-p38) in response to cellular stress and play a protective and pro-apoptotic role (5,15). Thus, UV-B is the main cause of inflammation in human keratinocytes via the MAPK pathways, JNK and p38 (16). The third includes the epidermal growth factor receptor (EGFR) pathway where UV-B-phosphorylated EGFR induces inflammation and skin tumorigenesis. Previous studies have demonstrated that EGFR regulates activation of p38 kinase leading to increased COX-2 and cytokine expressions (17,18).
The beneficial properties of mucus in UV protection have been established from research on fish. For example, coral reef fish can withstand UV due to mycosporine-like amino acids (MAAs) found in the external epithelial mucus that absorb UV (19). Relatively little is known regarding how mollusc mucus-derived compounds may mitigate UV-induced damage; yet, there is ample knowledge that molluscs, including abalone, snails, slugs, can survive in UV-exposed ecological niches. Molluscan mucus has increasingly been found to contain properties which are being exploited for use in medicines and cosmetics (20–23). For example, mucus-derived mucin compounds mixed with a honey gel were found to promote wound healing (24). Moreover, land snail (Achatina fulica