Fig 1: IGFBP-6 inhibits extracellular IGF-2 induced by oxidative stress in primary cortical neurons. Concentrations of (A) IGF-1 and (B) IGF-2 in the supernatant of primary cortical neuron cultures incubated with hMSC-CM or hMSC-CM pretreated with anti-IGFPB-6-Ab following H2O2 treatment were analyzed using an enzyme-linked immunosorbent assay. The data are presented the mean ± standard error of the mean of at least four independent experiments. *P<0.05 and **P<0.01 vs. control; †P<0.05 vs. H2O2; #P<0.05 vs. hMSC-CM. Analysis of variance followed by the Newman-Keuls post hoc test were used. hMSC-CM, human mesenchymal stem cell-conditioned medium; IGF, insulin-like growth factor; IGFBP-6 Ab, insulin-like growth factor binding protein-6 antibody.
Fig 2: IGFBP-6 activates Akt in oxidative stress-damaged primary cortical neurons via IGF-1 receptor-dependent signaling. (A) Phosphorylation of Akt was examined in primary cortical neurons incubated with hMSC-CM or hMSC-CM pretreated with an anti-IGFPB-6-Ab following H2O2 treatment. (B) Primary cortical neurons were pre-incubated with PPP (500 nM) for 15 min prior to H2O2 treatment. Expression levels of pAkt were detected 30 min following H2O2 treatment. Data are presented as the mean ± standard error of the mean of at least four independent experiments. **P<0.01, vs. control; ††P<0.01 vs. H2O2 (−) hMSC-CM; #P<0.05 and ##P<0.01 vs. H2O2 (+) hMSC-CM. Analysis of variance followed by the Newman-Keuls post hoc test were used. hMSC-CM, human mesenchymal stem cell-conditioned medium; pAKT, phosphorylated Akt; IGFBP-6 Ab, insulin-like growth factor binding protein 6 antibody; PPP, picropodophyllin.
Fig 3: Restoration of growth factors (GFs) and neurotrophic factors (NFs) in the brain ((A), n = 8–10/group) and muscles ((B), n = 8–10/group). Black: young animals (7 weeks old); red: aged animals; green: aged animals transplanted with F3 cells (1 × 106 cells every month); blue: aged animals transplanted with F3.ChAT cells (1 × 106 cells every month). BDNF: brain-derived neurotrophic factor. NGF: nerve growth factor. GDNF: glial cell-derived neurotrophic factor. VEGF: vascular endothelial growth factor. IGF-1: insulin-like growth factor-1. * Significantly different from young rats (p < 0.05). # Significantly different from aged rats (p < 0.05). + Significantly different from F3 treatment (p < 0.05).
Fig 4: Low-carbohydrate, high-fat and high-carbohydrate, low-fat diets impact the brain’s IGF and IGF-binding protein gene expression. (A) IGF-1 gene expression; (B) IGF-1 R gene expression; (C) IGFBP-2 gene expression; (D) IGFBP-5 gene expression Data were expressed as the mean ± SD. DEX, DEX + LCHF, and DEX + HCLF groups. DEX: rats treated with dexamethasone to induce MetS; DEX + LCHF: rats treated with dexamethasone to induce MetS and fed the low-carbohydrate, high-fat diet; DEX + HCLF: rats treated with dexamethasone to induce MetS and fed the high-carbohydrate, low-fat diet (applies to all figures). Y axis (Fold expression relative to control). Statistically significant if p ≤ 0.05 *; p < 0.01 **; p < 0.0001 ****. IGF-1: Insulin growth factor-1, IGF-1 R: Insulin growth factor-1 receptors, IGFBP-2: Insulin growth factor binding protein-1, and IGFBP-5: Insulin growth factor binding protein-5.
Fig 5: The impact of low-carbohydrate, high-fat and high-carbohydrate, low-fat diets on IGF and IGF-binding proteins serum level. (A) IGF-1 serum level; (B) IGFBP-2 serum level; (C) IGFBP-5 serum level. Data are expressed as mean ± SD. Statistically significant if p < 0.001 ***; p < 0.0001 ****. IGF-1: Insulin growth factor-1, IGFBP-2: Insulin growth factor binding protein-2, and IGFBP-5: Insulin growth factor binding protein-5.
Supplier Page from Abcam for Rat IGF-1 ELISA Kit