Molecular mechanism of the anti-inflammatory and skin protective effects of Syzygium formosum in human skin keratinocytes.

Irradiation injury, especially caused by UVB, of the skin is one of the critical reasons for skin inflammation and damage. The present study aimed to explore the protective effect of Syzygium formosum leafy extract (SFLE) and its mechanism of action against UVB-induced damages of human keratinocytes. In this study, SFLE was prepared from 100 kg dried leaves using industrial-scale processes. We found that SFLE markedly reduced markers of the skin inflammation in UVB-induced pro-inflammatory cytokines. Only 2 µg/mL of SFLE exhibited significantly stronger anti-inflammatory effects than the fivefold concentration of positive control. Intriguingly, an anti-inflammatory enzyme, heme oxygenase-1 expression was significantly induced by SFLE treatment. MMP-3 and -9 were, but not MMP-1, significantly reduced. SFLE inhibited the expression of the MAPK pathway, resulting in a decrease on UVB-induced reactive oxygen species. In conclusion, SFLE can potentially be used to treat skin inflammatory diseases. Supplementary Information: The online version contains supplementary material available at 10.1007/s10068-023-01380-4.

Preventive effects of inotodiol on polyinosinic-polycytidylic acid-induced inflammation in human dermal fibroblasts.

Double-strand RNA(dsRNA), which can induce inflammation, can be generated by necrotic keratinocytes in the skin environment. As an analog of dsRNA, polyinosinic-polycytidylic acid (poly(I:C)) is used to induce inflammation via the Toll-like Receptor 3 (TLR3) signaling pathway. Inotodiol, isolated from Inonotus obliquus, known as Chaga mushroom, is a natural lanostane-type triterpenoid with significant pharmacological activity and notable anti-inflammatory effects. However, the functions of inotodiol on dsRNA-induced inflammation in human dermal fibroblast (HDFs) remains unclear. In this study, we evaluated the anti-inflammatory effects of inotodiol inflammation induced on by poly(I:C) in HDFs. After pre-treatment with inotodiol, poly (I:C) was used to induce inflammation. Subsequently, mRNA expression and protein secretion of inflammatory cytokines, as well as TLR3 signaling protein levels were assessed. Inflammatory cytokines IL-1ß, IL-6, and TNF-α's increased mRNA expression by poly(I:C) in HDFs was significantly suppressed in the inotodiol pre-treatment group in a dose-dependent manner. A similar pattern was evaluated in the protein levels of these three cytokines. The inflammatory signals of TLR3 via p-IKK, p-p38, and NF-κB was reduced by inotodiol pre-treatment. Taken together, inotodiol possesses strong anti-inflammatory activity against poly(I:C)-induced inflammation in HDFs. Therefore, our findings support potential application of inotodiol as an effective anti-inflammatory agent in cosmetics.