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Basic Study
©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
Figure 6
Figure 6 Inhibition of microRNA-335-3p abolishes endothelial cell-exosomes-mediated protection against high glucose-induced ferroptosis in osteoblasts. A: The relative expression levels of mRNA for prostaglandin endoperoxide synthase 2 (PTGS2), glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), and solute carrier family 3 member 2 (SLC3A2) in each group of cells; B: Western blotting to detect the protein expressions of key ferroptosis markers PTGS2, GPX4, SLC7A11, SLC3A2; C: The relative protein expressions of PTGS2, GPX4, SLC7A11, SLC3A2. The bars indicate the mean ± SD from three independent experiments (n = 3). aP < 0.01 vs control, bP < 0.01 vs high glucose, cP < 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; PTGS2: Prostaglandin endoperoxide synthase 2; SLC3A2: Solute carrier family 3 member 2; SLC7A11: Solute carrier family 7 member 11; GPX4: Glutathione peroxidase 4; GAPDH: Glyceraldehyde 3-phosphate dehydrogenase.


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