Abstract
Long-term use of glucocorticoids is a widespread clinical problem, which currently has no effective solution other than discontinuing the use. Eicosapentaenoic acid (EPA), an omega-3 long chain polyunsaturated fatty acid (n-3 PUFA), which is largely contained in fish or fish oil, has been reported to promote cell viability and improve bone metabolism. However, little is known about the effects of EPA on dexamethasome (Dex)-induced cell apoptosis. In this study, we showed that EPA-induced autophagy of murine bone marrow-derived mesenchymal stem cells (mBMMSCs). Meanwhile, EPA, but not arachidonic acid (AA), markedly inhibited Dex-induced apoptosis and promoted the viability of mBMMSCs. We also observed that EPA-induced autophagy was modulated by GPR120, but not GPR40. Further experiments showed that the mechanism of EPA-induced autophagy associated with GPR120 modulation involved an increase in the active form of AMP-activated protein kinase and a decrease in the activity of mammalian target of RAPA. The protective effect of EPA on Dex-induced apoptosis via GPR120-meditated induction of adaptive autophagy was supported by in vivo experiments. In summary, our findings may have important implications in developing future strategies to use EPA in the prevention and therapy of the side effects induced by long-term Dex-abuse.
Highlights
Polyunsaturated fatty acids (PUFAs), which were for a long time solely considered as an energy source in our bodies, have been proven to be highly biologically active molecules
We showed that eicosapentaenoic acid (EPA)-induced autophagy of murine bone marrow-derived mesenchymal stem cells
GPR120 and GPR40 are G-protein coupled fatty acid receptors, and numerous studies have shown that EPA and arachidonic acid (AA) are endogenous ligands for these receptors,[7,8] which have been implicated in many key processes and exert multiple functions.[9,10,11]
Summary
Polyunsaturated fatty acids (PUFAs), which were for a long time solely considered as an energy source in our bodies, have been proven to be highly biologically active molecules. Attenuation of dexamethasome-induced apoptosis by eicosapentaenoic acid B Gao et al evidence suggests that EPA or AA can protect cells from apoptosis, the role of EPA in the induction of the autophagic pathway in mBMMSCs has not yet been examined. It is not known whether autophagy is induced in Dexinduced apoptosis and, if so, how autophagy contributes to cell apoptosis. Our results develop a better understanding of a unique mechanism of the protective action of EPA and GPR120 against side effects induced by long-term Dex use
Sign-in/Register to view highlights & summary 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.
