AI Article Synopsis
- The study investigates how Angelica polysaccharide (AP) can reduce oxidative damage in skin cells, which is important for preventing pressure ulcers.
- AP was found to improve cell survival and reduce apoptosis by activating key signaling pathways (PI3K/AKT and mTOR) and increasing levels of miR-126.
- The findings suggest that AP could serve as a potential therapeutic agent for enhancing skin health and safety in hospital settings.
Article Abstract
Background: Pressure ulcers (PUs) prevalence has been considered as an index for patient safety and cure quality of hospital and community. Skin cellular oxidative response damage is existed in the development of PUs. Angelica polysaccharide (AP) has the anti-oxidation function. Therefore, our goal was to investigate the mechanism of AP in relieving cellular oxidative damage.
Methods: Transfected HaCaT cells with miR-126 inhibitor, pre-treated by AP, and then treated by HO. CCK-8 assay and flow cytometry detection were set to test viability and apoptosis of cells respectively. qRT-PCR and western blot tested levels of miR-126 and oxidative damage relative factors. ROS assay tested the production of ROS in cells.
Results: Cellular oxidative response damage was induced by HO at concentration of 300 μM. We found that AP could attenuate cellular oxidative response damage caused by HO that it elevated cell viability, attenuated cell apoptosis and production of ROS and promoted activation of PI3K/AKT and mTOR signal pathways. Further, miR-126 was up-regulated by AP. The up-regulation of miR-126 could activate the PI3K/AKT and mTOR signal pathways.
Conclusion: Our study demonstrated that AP attenuated cellular oxidative response damage in HaCaT cells by positively regulated miR-126.
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| http://dx.doi.org/10.1016/j.yexmp.2019.104281 | DOI Listing |
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