Fig 1: Effects of DEX and LUT on BMSC osteogenesis, miR‐125b‐5p expression, and SIRT3/AMPK/mTOR axis. The administration of LUT restored the levels of RUNX2 (a), OSX (b), OPN (c), and OCN (d). Moreover, altered levels of miR‐125b‐5p expression (e), as well as gene expression and protein levels of SIRT3 (f, i), AMPK (g, j), and mTOR (h, k) were obtained after DEX and LUT treatment. p‐value < 0.05 was considered significant.
Fig 2: The expression of miR‐125b‐5p and SIRT3/AMPK/mTOR axis in animals with OP. DEX‐treated animals revealed overexpressed levels of miR‐125b‐5p (a). The gene expression and protein levels of SIRT3 (b, e) and AMPK (c, f) significantly reduced in the DEX group, while mTOR (d, g) was remarkably upregulated. LUT at a dose of 100 mg/kg/day ameliorated DEX‐induced alterations in miR‐125b‐5p expression and SIRT3/AMPK/mTOR axis. Similar lowercase letters on bars represent no significant difference between groups. p‐value < 0.05 was considered significant.
Fig 3: miR‐125b‐5p overexpression and SIRT3 downregulation inhibited therapeutic properties of LUT on DEX‐treated BMSCs. Specific mimics were used to overexpress miR‐125b‐5p and assess the effects of DEX and LUT on SIRT3/AMPK/mTOR axis (a), bone markers (b), and autophagic flux (c) in BMSCs. Moreover, SIRT3 expression was inhibited using specific siRNA, and the levels of AMPK/mTOR (d), bone (e), and autophagy (f) markers were evaluated. *: A significant difference with controls (CON). p‐value < 0.05 was considered significant.
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