igf 1r inhibitor treatment  (MedChemExpress)

Journal: bioRxiv

Article Title: Midazolam suppresses glioma progression by attenuating neuronal activity and downregulating IGF1 signaling

doi: 10.64898/2026.03.31.715727

Figure Lengend Snippet: (A) Differentially expressed genes and overall expression trends of cortical neurons from seven different groups. “D vs A”: log₂FC of KCls vs Control, “G vs D”: log₂FC of MDZs vs KCls. (B) Gene expression profiles of commonly secreted neuronal factors under KCl, and MDZ conditions. IGF1 is highlighted by a red dashed line. (C) Validation of IGF1and BDNF expression by RT-qPCR. n.s. P >0.05, * P < 0.05, ** P < 0.01, **** P < 0.0001. n=3. (D-E) Representative images and quantification of EdU assay after IGFBP3 experiment in GL261 cells. Scale bar = 100 μm. (F-G) Representative images and quantification of EdU assay after Linsitinib (OSI-906) treated experiments in GL261 cells. Scale bar = 200 μm. (H-I) Activation of the IGF1 downstream PI3K/AKT signaling pathway in glioma cells and its quantitative analysis. (J-K) PI3K/AKT signaling pathway change after IGFBP3 incubation in glioma cells. n.s. P >0.05, * P< 0.05, ** P< 0.01, *** P< 0.001, **** P< 0.0001. n=3.

Article Snippet: After 24 h incubation in Neu-CMs with or without 1ug/ml IGF1 binding protein-3 (Sigma, USA) [ ] , 100 μM IGF 1R inhibitor Linsitinib (OSI-906) (Sellect, USA) [ , ] or exogenous IGF1 factor (MCE, USA), the proliferation of glioma cells was detected by EdU assay.

Techniques: Expressing, Control, Gene Expression, Biomarker Discovery, Quantitative RT-PCR, EdU Assay, Activation Assay, Incubation

Journal: Journal of Advanced Research

Article Title: Novel function of macrophage migration inhibitory factor in regulating post-infarct inflammation and the therapeutic significance

doi: 10.1016/j.jare.2025.05.030

Figure Lengend Snippet: Macrophage migration inhibitory factor (MIF) promotes inflammatory cell migration and infiltration through C – C motif chemokine receptor 2 (CCR2) and C-X-C motif chemokine receptor (CXCR) 4 and promotes splenic monocyte mobilization via interaction with angiotensin Ⅱ type 1 receptor (AT-1R) after myocardial infarction (MI). A, peripheral blood mononuclear cells (PBMCs) chemotaxis in response to homogenized sham or infarct heart tissue from wild type (WT) mice at day 3 post-MI, or MI homogenate together with inhibition of C–C motif chemokine receptor 2 (CCR2), C-X-C motif chemokine receptor (CXCR) 2 and CXCR4, respectively. Cells/HPF, cells/high power field. PBMCs harvested from WT mice at 3 days post-MI. CCR2i, CCR2 inhibition. CXCR2i, CXCR2 inhibition. CXCR4i, CXCR4 inhibition. n = 4–8 per group. *** P < 0.001 vs. sham . B, PBMCs chemotaxis in response to recombinant human MIF (rMIF) or rMIF with inhibition of CCR2, CXCR2 and CXCR4, respectively. PBMCs harvested from WT mice at 3 days post-MI. n = 4–8 per group. *** P < 0.001 vs. control . C, Representative immunoblotting images for monocyte chemoattractant protein-1 (MCP-1), CXCR4 and internal reference protein (heat shock protein 60, HSP-60) in hearts from WT and global MIF deficient (MIFKO) mice with sham-operation or 72 h MI. D-E, Quantitative analysis of MCP-1 and CXCR4 expression. n = 6–9 per group. ** P < 0.01 vs. sham in the same genotype. *** P < 0.001 vs. sham in the same genotype. F, Splenic monocyte (from normal WT mice) chemotaxis in response to plasma from normal mice or mice with 1.5 h MI, or MI plasma together with losartan. Lor, losartan, AT-1R inhibitor. n = 6–8 per group. *** P < 0.001 vs. normal. G, Splenic monocytes (from normal WT mice) chemotaxis in response to rMIF and angiotensin II (Ang II), or together with losartan addition, respectively. n = 6–8 per group. ** P < 0.01 vs. Control. *** P < 0.001 vs. Control. H, Representative immunoblotting images for AT-1R and internal reference protein (HSP-60) in spleens from WT and global MIF deficient (MIFKO) mice with sham-operation and 1.5 h MI. I, Quantitative analysis of AT-1R expression. n = 8 per group. *** P < 0.001 vs. sham in the same genotype . J. Co-immunoprecipitation (Co-IP) assay using an anti-AT-1R antibody or IgG demonstrated the interaction between AT-1R and MIF, as well as between AT-1R and CD74 in splenic monocytes and spleen tissue. Input, input sample. IgG, negative control sample. IP, Co-IP sample.

Article Snippet: For all groups, splenic monocytes were pre-treated for 1 h using DMEM with or without AT-1R inhibitor (losartan, 10 μM, MedChemExpress) and 2 × 10 5 cells in 500 μl were added to the top chamber insert and then were processed following the same protocol as outlined for the PBMCs.

Techniques: Migration, Chemotaxis Assay, Inhibition, Recombinant, Control, Western Blot, Expressing, Clinical Proteomics, Co-Immunoprecipitation Assay, Negative Control

Journal: Journal of Nanobiotechnology

Article Title: RVG-targeted extracellular vesicles loaded with echinatin attenuate dopaminergic neurodegeneration via the IGF-2/PI3K/Akt pathway in Parkinson’s disease mice

doi: 10.1186/s12951-025-03997-5

Figure Lengend Snippet: RVG-EVs@Echi attenuate oxidative stress in the in vitro PD models. ( a ) Representative blots and ( b ) quantification of the expression levels of IGF2, P-PI3K, PI3K, P-Akt, Akt, and Nrf2 in MN9D cells. ( c ) Representative blots and ( d ) quantification of Bcl-2, Bax, and the resulting Bcl-2/Bax ratio in MN9D cells. ( e , g ) Representative blots and ( f , h ) quantification showing the effects of the IGF-1R/IR inhibitor NVP-AEW541 in MN9D cells. ( i ) Representative graphs of ROS generation in control or MPP+-treated cells upon RVG-EVs@Echi treatment. Scale bars, 50 μm and 10 μm for the original and magnified images, respectively. ( k ) MitoSOX was used to stain live control or MPP+-treated cells upon treatment with RVG-EVs@Echi. Scale bars, 50 μm and 10 μm for the original and magnified images, respectively. ( j , l ) Quantification of the relative ROS and MitoSOX fluorescence intensity. n = 6 per group. ( m ) Representative flow cytometry histograms and ( n ) quantification of mean fluorescence intensity (MFI) showing intracellular ROS levels in MN9D cells. n = 3 per group. Statistical Analysis: For (a-d): Groups are Control, MPP+, and MPP + + RVG-EVs@Echi. n = 3 per group. * p < 0.05, ** p < 0.01 vs. Control group; # p < 0.05, ## p < 0.01 vs. MPP + group. For (e-h): Groups are Control, MPP + + RVG-EVs@Echi, and MPP + + RVG-EVs@Echi + NVP-AEW541. n = 3 per group. * p < 0.05, ** p < 0.01 vs. Control group; # p < 0.05, ## p < 0.01 vs. MPP + + RVG-EVs@Echi group. For (i-n): Groups are Control, RVG-EVs@Echi, MPP+, and MPP + + RVG-EVs@Echi. * p < 0.05, ** p < 0.01 vs. Control group; # p < 0.05, ## p < 0.01 vs. RVG-EVs@Echi group; & p < 0.05, && p < 0.01 vs. MPP + group

Article Snippet: To assess the effects of RVG-EVs@Echi, MN9D cells were treated with MPP+ (600 μM) or RVG-EVs@Echi (1 μM) for 24 h. For the IGF-1R inhibition experiment, cells were pre-treated with the IGF-1R/IR inhibitor NVP-AEW541 (0.2 μM; MCE, HY-50866) [ ] for 2 h, followed by co-incubation with MPP + and RVG-EVs@Echi for 24 h.

Techniques: In Vitro, Expressing, Control, Staining, Fluorescence, Flow Cytometry