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cgrp powder  (MedChemExpress)


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    Structured Review

    MedChemExpress cgrp powder
    <t>CGRP</t> suppresses corneal tissue inflammation following alkali burn. ( A ) The volcano plot displayed the upregulated and downregulated genes in the corneas of mice from the CGRP-treated group compared with <t>the</t> <t>PBS-treated</t> group at 7 days post-injury ( n = 3). ( B ) The heatmap showed the differentially expressed genes in the corneas of mice from the CGRP-treated group compared with the PBS-treated group at 7 days post-injury ( n = 3). ( C ) The mRNA expression of the inflammatory factors IL-1β, iNOS, MCP-1, MMP3, and MMP9 was detected by qPCR on day 7 post-injury following CGRP treatment ( n = 4). ( D, E ) Representative flow cytometry plots and bar charts of CD45+ cells in the cornea after 7 days of treatment with CGRP following injury. ( F, G ) Representative micrographs and bar charts of macrophages in the cornea after 7 days treatment with topical CGRP or PBS ( n = 4). ( H ) Corneal macrophages were determined by flow cytometry ( n = 4). ( I, J ) Representative flow cytometry plots and bar charts of CD206+ macrophages in the cornea of the CGRP treatment group ( n = 4). ( K, L ) Representative micrographs and bar charts of neutrophils in the cornea after 7 days treatment with topical CGRP or PBS ( n = 4). (M) Corneal neutrophils were determined by flow cytometry ( n = 4). Data are shown as mean ± SD. ns: not significant; * P < 0.05; ** P < 0.01; *** P < 0.001.
    Cgrp Powder, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Corneal Nerves Promote Alkali Burn Repair by Modulating Macrophages and Neutrophils via Calcitonin Gene-Related Peptide"

    Article Title: Corneal Nerves Promote Alkali Burn Repair by Modulating Macrophages and Neutrophils via Calcitonin Gene-Related Peptide

    Journal: Investigative Ophthalmology & Visual Science

    doi: 10.1167/iovs.67.4.60

    CGRP suppresses corneal tissue inflammation following alkali burn. ( A ) The volcano plot displayed the upregulated and downregulated genes in the corneas of mice from the CGRP-treated group compared with the PBS-treated group at 7 days post-injury ( n = 3). ( B ) The heatmap showed the differentially expressed genes in the corneas of mice from the CGRP-treated group compared with the PBS-treated group at 7 days post-injury ( n = 3). ( C ) The mRNA expression of the inflammatory factors IL-1β, iNOS, MCP-1, MMP3, and MMP9 was detected by qPCR on day 7 post-injury following CGRP treatment ( n = 4). ( D, E ) Representative flow cytometry plots and bar charts of CD45+ cells in the cornea after 7 days of treatment with CGRP following injury. ( F, G ) Representative micrographs and bar charts of macrophages in the cornea after 7 days treatment with topical CGRP or PBS ( n = 4). ( H ) Corneal macrophages were determined by flow cytometry ( n = 4). ( I, J ) Representative flow cytometry plots and bar charts of CD206+ macrophages in the cornea of the CGRP treatment group ( n = 4). ( K, L ) Representative micrographs and bar charts of neutrophils in the cornea after 7 days treatment with topical CGRP or PBS ( n = 4). (M) Corneal neutrophils were determined by flow cytometry ( n = 4). Data are shown as mean ± SD. ns: not significant; * P < 0.05; ** P < 0.01; *** P < 0.001.
    Figure Legend Snippet: CGRP suppresses corneal tissue inflammation following alkali burn. ( A ) The volcano plot displayed the upregulated and downregulated genes in the corneas of mice from the CGRP-treated group compared with the PBS-treated group at 7 days post-injury ( n = 3). ( B ) The heatmap showed the differentially expressed genes in the corneas of mice from the CGRP-treated group compared with the PBS-treated group at 7 days post-injury ( n = 3). ( C ) The mRNA expression of the inflammatory factors IL-1β, iNOS, MCP-1, MMP3, and MMP9 was detected by qPCR on day 7 post-injury following CGRP treatment ( n = 4). ( D, E ) Representative flow cytometry plots and bar charts of CD45+ cells in the cornea after 7 days of treatment with CGRP following injury. ( F, G ) Representative micrographs and bar charts of macrophages in the cornea after 7 days treatment with topical CGRP or PBS ( n = 4). ( H ) Corneal macrophages were determined by flow cytometry ( n = 4). ( I, J ) Representative flow cytometry plots and bar charts of CD206+ macrophages in the cornea of the CGRP treatment group ( n = 4). ( K, L ) Representative micrographs and bar charts of neutrophils in the cornea after 7 days treatment with topical CGRP or PBS ( n = 4). (M) Corneal neutrophils were determined by flow cytometry ( n = 4). Data are shown as mean ± SD. ns: not significant; * P < 0.05; ** P < 0.01; *** P < 0.001.

    Techniques Used: Expressing, Flow Cytometry

    Expression of the CGRP receptor in neutrophils and macrophages, and transcriptomic analysis of macrophages following CGRP treatment in vitro. ( A, B ) Light microscope image of bone marrow-derived macrophages and bone marrow-derived neutrophils ( n = 4). ( C ) CALCRL and RAMP1 expression was detected in bone marrow-derived macrophages and neutrophils using immunostaining. Green = CALCRL, red = RAMP1 ( n = 4). ( D ) Heatmap of selected significantly upregulated and downregulated genes depicting standardized gene expression values in CGRP-treated cells compared to PBS-treated cells. The colored circles next to the heatmap denote gene functions. ( E ) Volcano plot displaying upregulated and downregulated genes in macrophages from the CGRP-treated group versus the PBS-treated group. ( F ) GO enrichment analysis of significantly upregulated ( red ) and downregulated ( blue ) genes in CGRP-treated and saline-treated macrophages.
    Figure Legend Snippet: Expression of the CGRP receptor in neutrophils and macrophages, and transcriptomic analysis of macrophages following CGRP treatment in vitro. ( A, B ) Light microscope image of bone marrow-derived macrophages and bone marrow-derived neutrophils ( n = 4). ( C ) CALCRL and RAMP1 expression was detected in bone marrow-derived macrophages and neutrophils using immunostaining. Green = CALCRL, red = RAMP1 ( n = 4). ( D ) Heatmap of selected significantly upregulated and downregulated genes depicting standardized gene expression values in CGRP-treated cells compared to PBS-treated cells. The colored circles next to the heatmap denote gene functions. ( E ) Volcano plot displaying upregulated and downregulated genes in macrophages from the CGRP-treated group versus the PBS-treated group. ( F ) GO enrichment analysis of significantly upregulated ( red ) and downregulated ( blue ) genes in CGRP-treated and saline-treated macrophages.

    Techniques Used: Expressing, In Vitro, Light Microscopy, Derivative Assay, Immunostaining, Gene Expression, Saline

    Related Articles

    Sterility:

    Article Title: Corneal Nerves Promote Alkali Burn Repair by Modulating Macrophages and Neutrophils via Calcitonin Gene-Related Peptide
    Article Snippet: .. We dissolved CGRP powder (HY-P0203; MedChenExpress) in sterile PBS to a final concentration of 50 μM, aliquoted it, and stored it at –80°C. ..

    Concentration Assay:

    Article Title: Corneal Nerves Promote Alkali Burn Repair by Modulating Macrophages and Neutrophils via Calcitonin Gene-Related Peptide
    Article Snippet: .. We dissolved CGRP powder (HY-P0203; MedChenExpress) in sterile PBS to a final concentration of 50 μM, aliquoted it, and stored it at –80°C. ..

    other:

    Article Title: Calcitonin gene-related peptide inhibits macrophage migration and differentiation via the GTPase Rap1
    Article Snippet: Selected sections were stained using haematoxylin and eosin (HE,Sigma-Aldrich), tartrate-resistant acid phosphatase (TRAP,Sigma-Aldrich), and Trichrome Stain (Masson) kits (Sigma-Aldrich) according to the manufacturer’s instructions.

    Article Title: CGRP alleviates epilepsy via JAK1-STAT1-P2RX7 signaling: a novel neuroprotective axis targeting neuronal damage.
    Article Snippet: Background: Calcitonin gene-related peptide (CGRP), a 37-amino-acid neuropeptide, is widely distributed in the central and peripheral nervous systems and participates in regulating various physiological and pathological processes such as vasodilation, inflammation, and pain.. Recent studies have shown that CGRP also exhibits neuroprotective effects, however, its role in epileptic neuronal damage remains unclear.. Methods: We conducted experiments on kainic acid (KA)-induced epileptic mice in vivo and glutamate induced neuronal cell death models in vitro, with treatments of CGRP and agonists or inhibitors of the corresponding receptors and pathway proteins.

    Article Title: Sensory-neuron-derived CGRPα controls white adipocyte differentiation and tissue plasticity
    Article Snippet: CGRPα , MedChemExpress , Cat#HY-P0203.

    Expressing:

    Article Title: Trigeminal nerve root compression induced neuroinflammatory response promotes mechanical allodynia through the CGRP/SP-Piezo2 axis via Ca 2+ signaling.
    Article Snippet: For hydrolysates, ADP (500 M, MCE, Cat# 257 HY-W010918) and adenosine (500 M, MCE, Cat# HY-B0228) were added to the 258 neuron cultures and incubated for 3 d. To identify signal transduction mechanisms and 259 transcription factors that regulate ATP-induced Piezo2 expression, inhibitors were 260 added and coincubated with ATP for 1 h. After changing the medium, the neurons were 261 treated with inhibitors for 72 h. The inhibitors that were used in this study includes T-262 5224 (50 M, APExBIO, Cat# B4664), 666-15 (100 nM, MCE Cat# HY-101120), BI-263 6015 (1.25 M, MCE, Cat# HY-108469), YC-1 (10 M, APExBIO, Cat# B7641), 264 cyclic pifithrin-α hydrobromide (20 M, APExBIO, Cat# A4477), SGC-CBP30 (100 265 nM, MCE, Cat# HY-15826), Go 6983 (100 nM, MCE, Cat# HY-13689), H89 (1 M, 266 APExBIO, Cat# B2190), SP600125 (1 M, MCE, Cat# HY-12041), SB203580 (10 M, 267 AR TIC LE IN PR ES S MCE, Cat# HY-10256A) and U0126 (10 M, MCE, Cat# HY-12031). .. Furthermore, α268 -CGRP (100 nM, MCE, Cat# HY-P0203) and Substance P (1 M, MCE, Cat# HY-269 P0201) were added to the neuronal cultures and manitained for 3 days to assess their 270 effects on Piezo2 expression. .. 271 RNA extraction and quantitative RT‒PCR analysis 272 Primary TG neurons were treated with ATP (2 mM/mL) for 1 h followed by culture 273 in fresh medium for an additional 1 h. Total RNA was subsequently extracted with 274 TRIzol reagent (Invitrogen, Cat #155596026).



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    Image Search Results


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    Article Title: A biomimetic hybrid membrane vesicle nanoplatform attenuates tendinopathy through neuroinflammation modulation and tendon regeneration

    doi: 10.1016/j.xcrm.2026.102937

    Figure Lengend Snippet:

    Article Snippet: Rabbit Polyclonal anti-CGRP , ABclonal , Cat# A5542; RRID: AB_2766323.

    Techniques: Recombinant, Lysis, Hydroxyproline Assay, Enzyme-linked Immunosorbent Assay, Isolation, SYBR Green Assay, Bicinchoninic Acid Protein Assay, Staining, Software

    Generation of iPSC line BO-VC1 -derived nociceptive neurons. Differentiation of ( A ) human iPSC line BO-VC1 into nociceptive neurons was done by dual SMAD inhibition, suppressing TGF-ß and BMP4 signaling, in knockout serum replacement (KSR) medium (day 0–4). This was followed by an overlapping inhibition of glycogen synthase kinase-3ß (GSK-3ß), vascular endothelial growth factor (VEGF), and Notch signaling (day 2–12), with KSR medium incremented with N2/B27 medium every second day by 25% from day 4 on. After reseeding of the ( B ) immature sensory neurons, final maturation was performed in N2/B27 medium infused with the neurotrophic factors glial cell line-derived neurotrophic factor (GDNF), nerve growth factor (NGF), and brain-derived neurotrophic factor (BDNF) (day 13 - approx. 60) according to the protocols of Chambers and Schoepf leading to the differentiation of ( C ) intermediate and finally ( D ) mature nociceptors (Scale bar: 500 μm). Mature nociceptive neurons express ( E ) the neuron specific microtubule element βIII-tubulin (βIIITUB) and vGLUT2, the sensory neuron markers ( F ) insulin gene enhancer protein 1 (ISL1) as well as the brain-specific homeobox/POU domain protein 3 A (BRN3A). Additionally, iPSC-derived differentiated cells express the nociceptive markers ( G ) transient receptor potential cation channel subfamily V member 1(TRPV1), H voltage-gated sodium ion channel 1.9 (Na V 1.9) and I TWIK-related spinal cord potassium channel (TRESK). Moreover, co-expression of ( J ) the calcitonin gene-related peptide (CGRP), the nociceptive marker high affinity nerve growth factor receptor (TRKA) and the estrogen receptor G-protein coupled estrogen receptor 1 (GPER1) was confirmed (Scale bars: 50 μm) ( K ) Quantification of the percentage of positive cells for the respective markers was 95.96 ± 2,495% for CGRP, 89.68 ± 6,137% for GPER1, 91.67 ± 5.270% for Na V 1.9, 95.83 ± 4.167% for TRKA, 80.38 ± 7.143% for TRPV1 and 98.55 ± 0.2899% for TRESK. L Realtime-PCR analysis in order to quantify nociceptive neuron marker and GPER1 gene expression of HDFa-derived iPSCs (line BO-VC1) and corresponding nociceptive neurons relative to HDFa cell samples mean value. Means ± SEM (standard error of the mean) from three independent passages were statistically analyzed by one-way ANOVA with Turkey’s multiple comparison test (L). n = 3 (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001)

    Journal: Stem Cell Research & Therapy

    Article Title: Activation of the G-protein coupled estrogen receptor 1 (GPER1) reduces transient receptor potential vanilloid 1 (TRPV1) activity and human iPSC-derived nociceptive neuron firing

    doi: 10.1186/s13287-026-05174-3

    Figure Lengend Snippet: Generation of iPSC line BO-VC1 -derived nociceptive neurons. Differentiation of ( A ) human iPSC line BO-VC1 into nociceptive neurons was done by dual SMAD inhibition, suppressing TGF-ß and BMP4 signaling, in knockout serum replacement (KSR) medium (day 0–4). This was followed by an overlapping inhibition of glycogen synthase kinase-3ß (GSK-3ß), vascular endothelial growth factor (VEGF), and Notch signaling (day 2–12), with KSR medium incremented with N2/B27 medium every second day by 25% from day 4 on. After reseeding of the ( B ) immature sensory neurons, final maturation was performed in N2/B27 medium infused with the neurotrophic factors glial cell line-derived neurotrophic factor (GDNF), nerve growth factor (NGF), and brain-derived neurotrophic factor (BDNF) (day 13 - approx. 60) according to the protocols of Chambers and Schoepf leading to the differentiation of ( C ) intermediate and finally ( D ) mature nociceptors (Scale bar: 500 μm). Mature nociceptive neurons express ( E ) the neuron specific microtubule element βIII-tubulin (βIIITUB) and vGLUT2, the sensory neuron markers ( F ) insulin gene enhancer protein 1 (ISL1) as well as the brain-specific homeobox/POU domain protein 3 A (BRN3A). Additionally, iPSC-derived differentiated cells express the nociceptive markers ( G ) transient receptor potential cation channel subfamily V member 1(TRPV1), H voltage-gated sodium ion channel 1.9 (Na V 1.9) and I TWIK-related spinal cord potassium channel (TRESK). Moreover, co-expression of ( J ) the calcitonin gene-related peptide (CGRP), the nociceptive marker high affinity nerve growth factor receptor (TRKA) and the estrogen receptor G-protein coupled estrogen receptor 1 (GPER1) was confirmed (Scale bars: 50 μm) ( K ) Quantification of the percentage of positive cells for the respective markers was 95.96 ± 2,495% for CGRP, 89.68 ± 6,137% for GPER1, 91.67 ± 5.270% for Na V 1.9, 95.83 ± 4.167% for TRKA, 80.38 ± 7.143% for TRPV1 and 98.55 ± 0.2899% for TRESK. L Realtime-PCR analysis in order to quantify nociceptive neuron marker and GPER1 gene expression of HDFa-derived iPSCs (line BO-VC1) and corresponding nociceptive neurons relative to HDFa cell samples mean value. Means ± SEM (standard error of the mean) from three independent passages were statistically analyzed by one-way ANOVA with Turkey’s multiple comparison test (L). n = 3 (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001)

    Article Snippet: Nevertheless, incubation with the first antibodies CGRP (1:500; # 414 004, Synaptic Systems GmbH, Göttingen, Germany), TRKA (1:500; # MA515509 , Thermo Fisher Scientific, Darmstadt, Germany), GPER1 (1:500; # ab39742, Abcam, ), BRN3A (1:100, # ab245230, Abcam, Cambridge, UK), ISL1 (1:100, #H00003670-M05, Abnova, Taipeh, Taiwan), TRPV1 (1:1000, # SAB5700857, Sigma-Aldrich, Merck, Darmstadt, Germany), vGlut2 (1:400, # MAB5504, Sigma-Aldrich, Merck, Darmstadt, Germany), ßIIITUB (1:300, # PA1-41331, Thermo Fisher Scientific, Darmstadt, Germany or 1:250, #302 304, Synaptic Systems GmbH, Göttingen, Germany) and Na V 1.9 (1:100, # ab65160, Abcam, Cambridge, UK) was done at 4 °C overnight.

    Techniques: Derivative Assay, Inhibition, Knock-Out, Expressing, Marker, Gene Expression, Comparison