Background
Polysaccharopeptides (PSPs) extracted from Trametes versicolor show antitumor, anti‐inflammatory, and immunomodulation effects. According to our previous report, the enzymatic hydrolysates obtained from T versicolor PSPs by 80 U/mL β‐1,3‐D‐glucanase (PSPs‐EH80) did not change the functional groups of PSPs but enhanced their antioxidative activities. However, the mechanism elevating the antioxidant and anti‐inflammatory effect of PSPs‐EH80 is not clear.
Aims
This research focused on the protective mechanism(s) of PSPs‐EH80 against free radical and 2,2'‐azobis (2‐amidinopropane) dihydrochloride (AAPH)‐induced oxidative damage in human keratinocyte (HaCaT) cells.
Methods
We evaluated the anti‐inflammatory potential of PSPs‐EH80 by assessing its free radical‐induced oxidative damage. Using the HaCaT cell as the experimental system, we tested the protective effects of PSPs‐EH80 on a model of AAPH‐induced cellular oxidative damage through the assessment of cell survival rate. Heme oxygenase 1 (HO‐1), nuclear factor erythroid 2‐related factor 2 (Nrf2), cyclooxygenase‐2 (COX‐2), nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB), extracellular signal‐regulated kinase (ERK), c‐Jun N‐terminal kinase (JNK) and p38 mitogen‐activated protein kinase were determined using MTT assays and Western blotting.
Results
We demonstrated that PSPs‐EH80 significantly enhanced keratinocyte viability, and augmented the antioxidant HO‐1 expressions through upregulation of the Nrf2, compared with PSPs. Furthermore, PSPs‐EH80 significantly reduced AAPH‐induced COX‐2 expressions through downregulation of the ERK, p38, and NF‐κB signaling pathways.
Conclusion
The PSPs‐EH80 exhibits a stronger antioxidant and anti‐inflammatory capacity than PSPs. Therefore, PSPs‐EH80 could be effective for attenuating free radical‐induced oxidative damage in human skin and can be applied widely in the fields of cosmetics and medicine.