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cgrp8 37  (MedChemExpress)


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    MedChemExpress cgrp8 37
    Cgrp8 37, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cgrp8 37/product/MedChemExpress
    Average 94 stars, based on 15 article reviews
    cgrp8 37 - by Bioz Stars, 2026-05
    94/100 stars

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    CGRP protects BMSCs from serum deprivation-induced apoptosis: (A) representative flow cytometric dot plots showing Annexin V-FITC/PI double staining after 24 and 48 h of serum-free culture. Four distinct cell populations are displayed: viable cells (Annexin V − /PI − , lower left quadrant), early apoptotic cells (Annexin V + /PI − , lower right quadrant), late apoptotic cells (Annexin V + /PI + , upper right quadrant), and necrotic cells (Annexin V − /PI + , upper left quadrant). Representative plots show control, CGRP (10 −8 M), CGRP + CGRP8-37 (10 −8 M CGRP + 10 −6 M CGRP8-37), and CGRP + H89 (10 −8 M CGRP + 0.2 μg/mL H89) treatment groups. (B) Quantitative analysis of the total apoptotic rate calculated as the sum of early apoptotic (Annexin V + /PI − ) and late apoptotic (Annexin V + /PI + ) cell percentages. CGRP treatment significantly reduced total apoptosis compared to control. CGRP8-37 and H89 co-treatments abolished CGRP’s protective effects, with apoptosis rates returning to control levels. Data represent mean ± SD from independent experiments (n = 6). *P < 0.05 compared to the control group; *P < 0.05 compared to the CGRP group using one-way ANOVA followed by Tukey’s post hoc test.

    Journal: Frontiers in Bioengineering and Biotechnology

    Article Title: CGRP-dependent molecular signaling drives bone marrow stem cell osteogenesis in distraction osteogenesis

    doi: 10.3389/fbioe.2025.1641476

    Figure Lengend Snippet: CGRP protects BMSCs from serum deprivation-induced apoptosis: (A) representative flow cytometric dot plots showing Annexin V-FITC/PI double staining after 24 and 48 h of serum-free culture. Four distinct cell populations are displayed: viable cells (Annexin V − /PI − , lower left quadrant), early apoptotic cells (Annexin V + /PI − , lower right quadrant), late apoptotic cells (Annexin V + /PI + , upper right quadrant), and necrotic cells (Annexin V − /PI + , upper left quadrant). Representative plots show control, CGRP (10 −8 M), CGRP + CGRP8-37 (10 −8 M CGRP + 10 −6 M CGRP8-37), and CGRP + H89 (10 −8 M CGRP + 0.2 μg/mL H89) treatment groups. (B) Quantitative analysis of the total apoptotic rate calculated as the sum of early apoptotic (Annexin V + /PI − ) and late apoptotic (Annexin V + /PI + ) cell percentages. CGRP treatment significantly reduced total apoptosis compared to control. CGRP8-37 and H89 co-treatments abolished CGRP’s protective effects, with apoptosis rates returning to control levels. Data represent mean ± SD from independent experiments (n = 6). *P < 0.05 compared to the control group; *P < 0.05 compared to the CGRP group using one-way ANOVA followed by Tukey’s post hoc test.

    Article Snippet: Rat α-calcitonin gene-related peptide (rat α-CGRP, HY-P0203), CGRP receptor antagonist rat CGRP8-37 (HY-P0209), and PKA inhibitor H89 (HY-15979) were purchased from MCE (China).

    Techniques: Double Staining, Control

    CGRP enhances BMSC osteogenic differentiation: (A) Alizarin Red S staining showing calcium nodule formation at days 14 and 21 of osteogenic induction. CGRP treatment resulted in more numerous and deeper-stained orange-red calcified nodules compared to controls. CGRP8-37 and H89 treatments significantly reduced CGRP-induced mineralization enhancement (scale bars: 50 μm). (B) Quantitative analysis of Alizarin Red staining using the cetylpyridinium chloride (CPC) extraction method. CGRP treatment showed 3.7-fold and 3.5-fold increases in mineralization at 14 and 21 days, respectively, compared to controls. Both CGRP8-37 and H89 treatments effectively blocked CGRP-induced mineralization enhancement. (C) Alkaline phosphatase (ALP) staining demonstrating enhanced early osteogenic marker expression at days 4 and 7. Purple precipitates indicate ALP activity (scale bars: 50 μm). CGRP8-37 and H89 treatments inhibited CGRP-induced osteogenic enhancement. (D) Quantitative ALP activity measurements normalized to total protein content. CGRP treatment demonstrated 3.7-fold and 3.9-fold increases in ALP activity at 4 and 7 days, respectively, compared to controls. CGRP + CGRP8-37 and CGRP + H89 groups showed significantly reduced ALP activity compared to CGRP alone, confirming that both receptor blockade and PKA pathway inhibition prevent CGRP’s osteogenic enhancing effects.

    Journal: Frontiers in Bioengineering and Biotechnology

    Article Title: CGRP-dependent molecular signaling drives bone marrow stem cell osteogenesis in distraction osteogenesis

    doi: 10.3389/fbioe.2025.1641476

    Figure Lengend Snippet: CGRP enhances BMSC osteogenic differentiation: (A) Alizarin Red S staining showing calcium nodule formation at days 14 and 21 of osteogenic induction. CGRP treatment resulted in more numerous and deeper-stained orange-red calcified nodules compared to controls. CGRP8-37 and H89 treatments significantly reduced CGRP-induced mineralization enhancement (scale bars: 50 μm). (B) Quantitative analysis of Alizarin Red staining using the cetylpyridinium chloride (CPC) extraction method. CGRP treatment showed 3.7-fold and 3.5-fold increases in mineralization at 14 and 21 days, respectively, compared to controls. Both CGRP8-37 and H89 treatments effectively blocked CGRP-induced mineralization enhancement. (C) Alkaline phosphatase (ALP) staining demonstrating enhanced early osteogenic marker expression at days 4 and 7. Purple precipitates indicate ALP activity (scale bars: 50 μm). CGRP8-37 and H89 treatments inhibited CGRP-induced osteogenic enhancement. (D) Quantitative ALP activity measurements normalized to total protein content. CGRP treatment demonstrated 3.7-fold and 3.9-fold increases in ALP activity at 4 and 7 days, respectively, compared to controls. CGRP + CGRP8-37 and CGRP + H89 groups showed significantly reduced ALP activity compared to CGRP alone, confirming that both receptor blockade and PKA pathway inhibition prevent CGRP’s osteogenic enhancing effects.

    Article Snippet: Rat α-calcitonin gene-related peptide (rat α-CGRP, HY-P0203), CGRP receptor antagonist rat CGRP8-37 (HY-P0209), and PKA inhibitor H89 (HY-15979) were purchased from MCE (China).

    Techniques: Staining, Extraction, Marker, Expressing, Activity Assay, Inhibition

    CGRP activates the cAMP/PKA signaling pathway in BMSCs: (A) ELISA quantification of intracellular cAMP levels 30 min post-treatment. CGRP rapidly increased cAMP concentration, blocked by CGRP8-37 and H89. Data represent mean ± SD (n = 6). (B-D) Western blot analysis of PKA and CREB phosphorylation at 30 min. Representative blots and quantitative analysis of p-PKA/PKA and p-CREB/CREB ratios. Data represent mean ± SD. *P < 0.05.

    Journal: Frontiers in Bioengineering and Biotechnology

    Article Title: CGRP-dependent molecular signaling drives bone marrow stem cell osteogenesis in distraction osteogenesis

    doi: 10.3389/fbioe.2025.1641476

    Figure Lengend Snippet: CGRP activates the cAMP/PKA signaling pathway in BMSCs: (A) ELISA quantification of intracellular cAMP levels 30 min post-treatment. CGRP rapidly increased cAMP concentration, blocked by CGRP8-37 and H89. Data represent mean ± SD (n = 6). (B-D) Western blot analysis of PKA and CREB phosphorylation at 30 min. Representative blots and quantitative analysis of p-PKA/PKA and p-CREB/CREB ratios. Data represent mean ± SD. *P < 0.05.

    Article Snippet: Rat α-calcitonin gene-related peptide (rat α-CGRP, HY-P0203), CGRP receptor antagonist rat CGRP8-37 (HY-P0209), and PKA inhibitor H89 (HY-15979) were purchased from MCE (China).

    Techniques: Enzyme-linked Immunosorbent Assay, Concentration Assay, Western Blot, Phospho-proteomics

    CGRP enhances biomechanical properties of regenerated bone: three-point bending test results at 6 weeks of consolidation showing (A) ultimate load, (B) energy to failure, and (C) stiffness measurements. CGRP treatment significantly improved all mechanical parameters compared to controls. CGRP8-37 and H89 abolished these beneficial effects. Data represent mean ± SD. *P < 0.05.

    Journal: Frontiers in Bioengineering and Biotechnology

    Article Title: CGRP-dependent molecular signaling drives bone marrow stem cell osteogenesis in distraction osteogenesis

    doi: 10.3389/fbioe.2025.1641476

    Figure Lengend Snippet: CGRP enhances biomechanical properties of regenerated bone: three-point bending test results at 6 weeks of consolidation showing (A) ultimate load, (B) energy to failure, and (C) stiffness measurements. CGRP treatment significantly improved all mechanical parameters compared to controls. CGRP8-37 and H89 abolished these beneficial effects. Data represent mean ± SD. *P < 0.05.

    Article Snippet: Rat α-calcitonin gene-related peptide (rat α-CGRP, HY-P0203), CGRP receptor antagonist rat CGRP8-37 (HY-P0209), and PKA inhibitor H89 (HY-15979) were purchased from MCE (China).

    Techniques: