AI Article Synopsis
- Oxidative damage from UVB rays significantly harms skin, and maslinic acid (MA), a natural compound, shows promise as an anti-inflammatory and antioxidant agent.
- The study investigated MA's effects on human foreskin fibroblast cells (HFF-1) facing oxidative stress from UVB radiation, assessing factors like cell growth, reactive oxygen species, and inflammation levels.
- Results indicated that MA improved cell viability, decreased harmful ROS levels, boosted antioxidant enzyme activity, and inhibited inflammation and NF-κB activation, suggesting MA's potential to mitigate UVB-induced oxidative damage.
Article Abstract
Background: Oxidative damage is one of the major mechanisms of ultraviolet B (UVB)-induced damage to the skin. Maslinic acid (MA) is a natural compound of pentacyclic triterpene acids. It has been proved to have anti-inflammatory and antioxidant properties.
Objective: This study aimed to explore the effects of MA on oxidative damage in human foreskin fibroblast cells (HFF-1) and the potential molecular mechanisms.
Methods: A specific dose of UVB radiation was used to induce oxidative damage in HFF-1. Based on this, we performed measurements of cell proliferation, reactive oxygen species (ROS) levels, antioxidant enzyme activity, inflammation-related mediators, and NF-κB nuclear localization with or without the addition of MA.
Results: MA significantly promoted cell proliferation viability at 10 and 20 μM. The addition of MA 24 h before UVB irradiation was more effective at enhancing cell proliferation and also produced lower ROS levels compared to co-cultured fibroblasts and MA for 24 h after irradiation. However, there was no statistically significant difference between groups at concentrations of 10 and 20 μM. The pretreatment group with MA had elevated superoxide dismutase and catalase activities, decreased IL-6 generation, and lowered mRNA levels of IL-6, TNF-α and MMP3 in comparison with the UVB-irradiated group without additional MA. Meanwhile, the nuclear translocation of NF-κB and the degradation of IκB were inhibited by MA pretreatment.
Conclusion: Taken together, these findings suggest that MA may alleviate UVB-induced oxidative damage in HFF-1 by inhibiting the nuclear translocation of NF-κB.
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| http://dx.doi.org/10.1111/jocd.15730 | DOI Listing |
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