©The Author(s) 2026.
World J Diabetes. Jan 15, 2026; 17(1): 111165
Published online Jan 15, 2026. doi: 10.4239/wjd.v17.i1.111165
Published online Jan 15, 2026. doi: 10.4239/wjd.v17.i1.111165
Figure 5 Inhibition of microRNA-335-3p abolishes endothelial cell-exosomes-mediated protection against high glucose-induced oxidative stress in osteoblasts.
A: Detection of microRNA-335-3p levels in osteoblasts induced by high glucose after inhibition of microRNA-335-3p by reverse trans cription-quantitative polymerase chain reaction; B-D: Results of reactive oxygen species, malondialdehyde and glutathione quantitative analysis; E: Detection of cellular reactive oxygen species levels in each group using dichlorofluorescein fluorescence probe. The bars indicate the mean ± SD from three independent experiments (n = 3). aP < 0.05 vs control, bP < 0.01 vs control, cP < 0.01 vs high glucose, dP < 0.01 vs high glucose + exosomes + negative control. Con: Osteoblasts treated with normal glucose; HG: Osteoblasts treated with high glucose; HG + Exos: High glucose + endothelial cell-exosomes; HG + Exos + NC: High glucose + negative control transfection + endothelial cell-exosomes; HG + Exos + inhibitor: High glucose + microRNA-335-3p inhibitor + endothelial cell-exosomes.
- Citation: Shao C, Zhang LJ, Song YL, Wang YQ, Zha XJ, Li J, Ye CS, Chen LL, Chen MW, Jin GX. Endothelial cell-derived exosomes inhibit high glucose-induced osteoblast ferroptosis by activating microRNA-335-3p/prostaglandin endoperoxide synthase 2. World J Diabetes 2026; 17(1): 111165
- URL: https://www.wjgnet.com/1948-9358/full/v17/i1/111165.htm
- DOI: https://dx.doi.org/10.4239/wjd.v17.i1.111165