Non-alcoholic steatohepatitis(NASH),an advanced form of non-alcoholic fatty liver disease(NAFLD),has emerged as the leading cause of liver failure and related death.Currently,no medication is specifically approved to ...Non-alcoholic steatohepatitis(NASH),an advanced form of non-alcoholic fatty liver disease(NAFLD),has emerged as the leading cause of liver failure and related death.Currently,no medication is specifically approved to treat NAFLD or NASH.Here we report that oral administration of honey vesiclelike nanoparticles(H-VLNs)to naturally aged mice protects the liver from NASH development.H-VLNs are dominantly taken up by Kupffer cells in the liver and suppress hepatic chronic inflammation and further development of fibrosis and nodule formation in aged mice.Besides their reported antiinflammasome function,H-VLNs are found to inhibit the transcriptional activities of C-JUN and nuclear factor-kappa B(NF-κB).MicroRNAs miR5119 and miR5108 and phenolic compound luteolin in H-VLNs are identified in suppressing both the C-JUN and NF-kB pathways.Collectively,oral intake of H-VLNs represents a promising new user-friendly modality to prevent the development of NASH.展开更多
基金supported by the United States Department of Agriculture(USDA)National Institute of Food and Agriculture(NIFA)Multistate Hatch Project 1021080,Standard Grant(2021-67017-34206,USA)the National Institutes of Health(NIH)grant R01DK124590(USA)+1 种基金partially funded by the Nebraska Center for Integrated Biomolecular Communication COBRE grant(P20 GM113126,NIGMS,USA)the Nebraska Research Initiative.
文摘Non-alcoholic steatohepatitis(NASH),an advanced form of non-alcoholic fatty liver disease(NAFLD),has emerged as the leading cause of liver failure and related death.Currently,no medication is specifically approved to treat NAFLD or NASH.Here we report that oral administration of honey vesiclelike nanoparticles(H-VLNs)to naturally aged mice protects the liver from NASH development.H-VLNs are dominantly taken up by Kupffer cells in the liver and suppress hepatic chronic inflammation and further development of fibrosis and nodule formation in aged mice.Besides their reported antiinflammasome function,H-VLNs are found to inhibit the transcriptional activities of C-JUN and nuclear factor-kappa B(NF-κB).MicroRNAs miR5119 and miR5108 and phenolic compound luteolin in H-VLNs are identified in suppressing both the C-JUN and NF-kB pathways.Collectively,oral intake of H-VLNs represents a promising new user-friendly modality to prevent the development of NASH.
