Abstract
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. Transfected HaCaT cells with miR-126 inhibitor, pre-treated by AP, and then treated by H2O2. 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. Cellular oxidative response damage was induced by H2O2 at concentration of 300 μM. We found that AP could attenuate cellular oxidative response damage caused by H2O2 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. Our study demonstrated that AP attenuated cellular oxidative response damage in HaCaT cells by positively regulated miR-126.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
