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trpv1  (Alomone Labs)


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    Structured Review

    Alomone Labs trpv1
    <t>TRPV1-mediated</t> nociceptive sensitization in the DRG and spinal cord dorsal horn (SC) following CCI and treatment. (A) Schematic illustration of the proposed mechanism: Injury-induced <t>TRPV1</t> ion channel activation triggers calcium influx and downstream CGRP release, which activates adenylate cyclase/PKA signaling to amplify neuropathic pain sensitization. (B) Representative immunofluorescence images of the DRG stained for TRPV1 (red), NeuN (green), and DAPI (blue). The Injury group shows marked up-regulation of TRPV1 in sensory neurons. Dex/Lid@PLX/HA treatment substantially reduces TRPV1 expression, restoring it to near-Naive levels. Scale bars, 200 μm (overview) and 50 μm (inset). (C) Immunofluorescence staining for TRPV1 (red) and NeuN (green) in the spinal dorsal horn. The dashed line indicates the dorsal horn boundary. Dex/Lid@PLX/HA significantly suppresses injury-induced central TRPV1 up-regulation. Scale bar, 200 μm. (D to F) Quantitative analysis of the relative TRPV1 + area in the DRG (top) and spinal cord (middle), and the SGC/neuron ratio. Dex/Lid@PLX/HA shows marked suppression of TRPV1 overexpression relative to the injury group. Data are presented as mean ± SEM. **** P < 0.0001, ** P < 0.01, * P < 0.05, ns: not significant.
    Trpv1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/trpv1+acc+030/Guinea+pig+Anti-TRPV1+(VR1)+Antibody/pmc13216820-86-14-15
    Average 93 stars, based on 18 article reviews
    trpv1 - by Bioz Stars, 2026-10
    93/100 stars

    Images

    1) Product Images from "Injectable Poloxamer and Hyaluronic Acid Hydrogel for Sustained Co-Delivery of Dexamethasone and Lidocaine Ameliorates Neuropathic Pain"

    Article Title: Injectable Poloxamer and Hyaluronic Acid Hydrogel for Sustained Co-Delivery of Dexamethasone and Lidocaine Ameliorates Neuropathic Pain

    Journal: Biomaterials Research

    doi: 10.34133/bmr.0373

    TRPV1-mediated nociceptive sensitization in the DRG and spinal cord dorsal horn (SC) following CCI and treatment. (A) Schematic illustration of the proposed mechanism: Injury-induced TRPV1 ion channel activation triggers calcium influx and downstream CGRP release, which activates adenylate cyclase/PKA signaling to amplify neuropathic pain sensitization. (B) Representative immunofluorescence images of the DRG stained for TRPV1 (red), NeuN (green), and DAPI (blue). The Injury group shows marked up-regulation of TRPV1 in sensory neurons. Dex/Lid@PLX/HA treatment substantially reduces TRPV1 expression, restoring it to near-Naive levels. Scale bars, 200 μm (overview) and 50 μm (inset). (C) Immunofluorescence staining for TRPV1 (red) and NeuN (green) in the spinal dorsal horn. The dashed line indicates the dorsal horn boundary. Dex/Lid@PLX/HA significantly suppresses injury-induced central TRPV1 up-regulation. Scale bar, 200 μm. (D to F) Quantitative analysis of the relative TRPV1 + area in the DRG (top) and spinal cord (middle), and the SGC/neuron ratio. Dex/Lid@PLX/HA shows marked suppression of TRPV1 overexpression relative to the injury group. Data are presented as mean ± SEM. **** P < 0.0001, ** P < 0.01, * P < 0.05, ns: not significant.
    Figure Legend Snippet: TRPV1-mediated nociceptive sensitization in the DRG and spinal cord dorsal horn (SC) following CCI and treatment. (A) Schematic illustration of the proposed mechanism: Injury-induced TRPV1 ion channel activation triggers calcium influx and downstream CGRP release, which activates adenylate cyclase/PKA signaling to amplify neuropathic pain sensitization. (B) Representative immunofluorescence images of the DRG stained for TRPV1 (red), NeuN (green), and DAPI (blue). The Injury group shows marked up-regulation of TRPV1 in sensory neurons. Dex/Lid@PLX/HA treatment substantially reduces TRPV1 expression, restoring it to near-Naive levels. Scale bars, 200 μm (overview) and 50 μm (inset). (C) Immunofluorescence staining for TRPV1 (red) and NeuN (green) in the spinal dorsal horn. The dashed line indicates the dorsal horn boundary. Dex/Lid@PLX/HA significantly suppresses injury-induced central TRPV1 up-regulation. Scale bar, 200 μm. (D to F) Quantitative analysis of the relative TRPV1 + area in the DRG (top) and spinal cord (middle), and the SGC/neuron ratio. Dex/Lid@PLX/HA shows marked suppression of TRPV1 overexpression relative to the injury group. Data are presented as mean ± SEM. **** P < 0.0001, ** P < 0.01, * P < 0.05, ns: not significant.

    Techniques Used: Activation Assay, Immunofluorescence, Staining, Expressing, Over Expression

    Related Articles

    Transfection:

    Article Title: Skin inflammation and itch response are independently regulated by distinct nociceptor subsets.
    Article Snippet: 4μm sections were stained with H&E, imaged using a LEICA DM4000B microscope and analyzed with Fiji. .. They were then Antibody Reference Atf3 NBP1-85816 (Novius) TH AB1542 (Merck) Tubb3 (b-tubulin) 801210 (Biolegend) IB4-488 I21411 (Thermofisher) Trpv1 ACC-030 (Alomone) Substance P MAB356 (Merck) Gfrα2 AF429 (Bio-Techne) P2X3R APR-026 (Alomone) NFH AB1989 (Merck) e4 Immunity 59, 1–16.e1–e9, May 12, 2026 transfected with 2 μg of TRPM8, TRPV1, TRPV4 or TRPA1 plus GCamp6 (0.3μg) using the calcium phosphate method. ..



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    <t>TRPV1-mediated</t> nociceptive sensitization in the DRG and spinal cord dorsal horn (SC) following CCI and treatment. (A) Schematic illustration of the proposed mechanism: Injury-induced <t>TRPV1</t> ion channel activation triggers calcium influx and downstream CGRP release, which activates adenylate cyclase/PKA signaling to amplify neuropathic pain sensitization. (B) Representative immunofluorescence images of the DRG stained for TRPV1 (red), NeuN (green), and DAPI (blue). The Injury group shows marked up-regulation of TRPV1 in sensory neurons. Dex/Lid@PLX/HA treatment substantially reduces TRPV1 expression, restoring it to near-Naive levels. Scale bars, 200 μm (overview) and 50 μm (inset). (C) Immunofluorescence staining for TRPV1 (red) and NeuN (green) in the spinal dorsal horn. The dashed line indicates the dorsal horn boundary. Dex/Lid@PLX/HA significantly suppresses injury-induced central TRPV1 up-regulation. Scale bar, 200 μm. (D to F) Quantitative analysis of the relative TRPV1 + area in the DRG (top) and spinal cord (middle), and the SGC/neuron ratio. Dex/Lid@PLX/HA shows marked suppression of TRPV1 overexpression relative to the injury group. Data are presented as mean ± SEM. **** P < 0.0001, ** P < 0.01, * P < 0.05, ns: not significant.
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    (A) Immunoblot analysis shows <t>TRPV1,</t> TRPA1, and actin levels in WT BMDMs 48 h following treatment with or without IL-4 plus GMCSF (25 ng/ml). (B-C) Densitometric quantification of immunoblot data from (A) (n = 3 biological replicates; one-way ANOVA, **p < 0.01, ***p < 0.001). (D) Representative immunofluorescence images of WT BMDMs stained for TRPV1 (red) <t>using</t> <t>anti-TRPV1</t> IgG (original magnification, 60 x; scale bar, 2 μm; n = 10 cells per condition). Statistical analysis by Student’s t-test, ***p < 0.001.
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    (A) Immunoblot analysis shows <t>TRPV1,</t> TRPA1, and actin levels in WT BMDMs 48 h following treatment with or without IL-4 plus GMCSF (25 ng/ml). (B-C) Densitometric quantification of immunoblot data from (A) (n = 3 biological replicates; one-way ANOVA, **p < 0.01, ***p < 0.001). (D) Representative immunofluorescence images of WT BMDMs stained for TRPV1 (red) <t>using</t> <t>anti-TRPV1</t> IgG (original magnification, 60 x; scale bar, 2 μm; n = 10 cells per condition). Statistical analysis by Student’s t-test, ***p < 0.001.
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    (A) Immunoblot analysis shows <t>TRPV1,</t> TRPA1, and actin levels in WT BMDMs 48 h following treatment with or without IL-4 plus GMCSF (25 ng/ml). (B-C) Densitometric quantification of immunoblot data from (A) (n = 3 biological replicates; one-way ANOVA, **p < 0.01, ***p < 0.001). (D) Representative immunofluorescence images of WT BMDMs stained for TRPV1 (red) <t>using</t> <t>anti-TRPV1</t> IgG (original magnification, 60 x; scale bar, 2 μm; n = 10 cells per condition). Statistical analysis by Student’s t-test, ***p < 0.001.
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    Image Search Results


    TRPV1-mediated nociceptive sensitization in the DRG and spinal cord dorsal horn (SC) following CCI and treatment. (A) Schematic illustration of the proposed mechanism: Injury-induced TRPV1 ion channel activation triggers calcium influx and downstream CGRP release, which activates adenylate cyclase/PKA signaling to amplify neuropathic pain sensitization. (B) Representative immunofluorescence images of the DRG stained for TRPV1 (red), NeuN (green), and DAPI (blue). The Injury group shows marked up-regulation of TRPV1 in sensory neurons. Dex/Lid@PLX/HA treatment substantially reduces TRPV1 expression, restoring it to near-Naive levels. Scale bars, 200 μm (overview) and 50 μm (inset). (C) Immunofluorescence staining for TRPV1 (red) and NeuN (green) in the spinal dorsal horn. The dashed line indicates the dorsal horn boundary. Dex/Lid@PLX/HA significantly suppresses injury-induced central TRPV1 up-regulation. Scale bar, 200 μm. (D to F) Quantitative analysis of the relative TRPV1 + area in the DRG (top) and spinal cord (middle), and the SGC/neuron ratio. Dex/Lid@PLX/HA shows marked suppression of TRPV1 overexpression relative to the injury group. Data are presented as mean ± SEM. **** P < 0.0001, ** P < 0.01, * P < 0.05, ns: not significant.

    Journal: Biomaterials Research

    Article Title: Injectable Poloxamer and Hyaluronic Acid Hydrogel for Sustained Co-Delivery of Dexamethasone and Lidocaine Ameliorates Neuropathic Pain

    doi: 10.34133/bmr.0373

    Figure Lengend Snippet: TRPV1-mediated nociceptive sensitization in the DRG and spinal cord dorsal horn (SC) following CCI and treatment. (A) Schematic illustration of the proposed mechanism: Injury-induced TRPV1 ion channel activation triggers calcium influx and downstream CGRP release, which activates adenylate cyclase/PKA signaling to amplify neuropathic pain sensitization. (B) Representative immunofluorescence images of the DRG stained for TRPV1 (red), NeuN (green), and DAPI (blue). The Injury group shows marked up-regulation of TRPV1 in sensory neurons. Dex/Lid@PLX/HA treatment substantially reduces TRPV1 expression, restoring it to near-Naive levels. Scale bars, 200 μm (overview) and 50 μm (inset). (C) Immunofluorescence staining for TRPV1 (red) and NeuN (green) in the spinal dorsal horn. The dashed line indicates the dorsal horn boundary. Dex/Lid@PLX/HA significantly suppresses injury-induced central TRPV1 up-regulation. Scale bar, 200 μm. (D to F) Quantitative analysis of the relative TRPV1 + area in the DRG (top) and spinal cord (middle), and the SGC/neuron ratio. Dex/Lid@PLX/HA shows marked suppression of TRPV1 overexpression relative to the injury group. Data are presented as mean ± SEM. **** P < 0.0001, ** P < 0.01, * P < 0.05, ns: not significant.

    Article Snippet: The sections were then incubated overnight at 4 °C with the following primary antibodies: TRPV1 (Alomone Labs, catalog number ACC-030-GP), Iba-1 (Abcam, catalog number ab5076), NeuN (Abcam, catalog number ab104224), CD68 (Abcam, catalog number ab31630), CD163 (Abcam, catalog number ab182422), CGRP (Abcam, catalog number ab47027), GFAP (Millipore, catalog number MAB360), and NF200 (Abcam, catalog number ab8135).

    Techniques: Activation Assay, Immunofluorescence, Staining, Expressing, Over Expression

    (A) Immunoblot analysis shows TRPV1, TRPA1, and actin levels in WT BMDMs 48 h following treatment with or without IL-4 plus GMCSF (25 ng/ml). (B-C) Densitometric quantification of immunoblot data from (A) (n = 3 biological replicates; one-way ANOVA, **p < 0.01, ***p < 0.001). (D) Representative immunofluorescence images of WT BMDMs stained for TRPV1 (red) using anti-TRPV1 IgG (original magnification, 60 x; scale bar, 2 μm; n = 10 cells per condition). Statistical analysis by Student’s t-test, ***p < 0.001.

    Journal: bioRxiv

    Article Title: A novel role for TRPV1 in macrophage giant cell formation

    doi: 10.64898/2026.05.11.724406

    Figure Lengend Snippet: (A) Immunoblot analysis shows TRPV1, TRPA1, and actin levels in WT BMDMs 48 h following treatment with or without IL-4 plus GMCSF (25 ng/ml). (B-C) Densitometric quantification of immunoblot data from (A) (n = 3 biological replicates; one-way ANOVA, **p < 0.01, ***p < 0.001). (D) Representative immunofluorescence images of WT BMDMs stained for TRPV1 (red) using anti-TRPV1 IgG (original magnification, 60 x; scale bar, 2 μm; n = 10 cells per condition). Statistical analysis by Student’s t-test, ***p < 0.001.

    Article Snippet: Primary antibodies comprised anti-actin (cat# 4970S; Cell Signaling Technology, Danvers, MA) and anti-TRPV1 (cat# ACC-030), anti-TRPV2 (cat# ACC-039), and anti-TRPA1 (cat# ACC-037) from Alomone Labs. Species-appropriate secondary antibodies (goat, rabbit, and mouse) were obtained from Jackson ImmunoResearch.

    Techniques: Western Blot, Immunofluorescence, Staining

    (A) Representative Giemsa-stained images of multinucleated FBGCs in WT BMDMs left untreated or stimulated with IL-4 plus GMCSF (25 ng/ml, 96 h), in the presence or absence of the TRPV1 antagonist AMG. (B-D) Quantitative analysis of FBGC formation from (A): (B) number of FBGCs per high-power field, (C) percentage of fused BMDMs, and (D) average FBGC size. Data represent n = 3 biological replicates with 5 images per group; scale bar, 100 μm; Student’s t-test, ***p < 0.001, ****p < 0.0001. (E) Representative immunofluorescence images of WT BMDMs transfected with scramble or TRPV1-targeting siRNA, stained for TRPV1 (red) using anti-TRPV1 IgG (original magnification, 60x; scale bar, 2 μm). (F) Quantification of TRPV1 fluorescence intensity (n = 10 cells per condition; Student’s t-test, ***p < 0.001). (G) Immunoblot showing TRPV1 expression in WT BMDMs 48 h after transfection with scramble or TRPV1 siRNA. (H-J) Quantification of FBGC formation following TRPV1 knockdown: (H) number of FBGCs per high-power field, (I) percentage of fused BMDMs, and (J) average FBGC size. Data represent n = 3 biological replicates with 5 images per group; Student’s t-test, ***p < 0.001.

    Journal: bioRxiv

    Article Title: A novel role for TRPV1 in macrophage giant cell formation

    doi: 10.64898/2026.05.11.724406

    Figure Lengend Snippet: (A) Representative Giemsa-stained images of multinucleated FBGCs in WT BMDMs left untreated or stimulated with IL-4 plus GMCSF (25 ng/ml, 96 h), in the presence or absence of the TRPV1 antagonist AMG. (B-D) Quantitative analysis of FBGC formation from (A): (B) number of FBGCs per high-power field, (C) percentage of fused BMDMs, and (D) average FBGC size. Data represent n = 3 biological replicates with 5 images per group; scale bar, 100 μm; Student’s t-test, ***p < 0.001, ****p < 0.0001. (E) Representative immunofluorescence images of WT BMDMs transfected with scramble or TRPV1-targeting siRNA, stained for TRPV1 (red) using anti-TRPV1 IgG (original magnification, 60x; scale bar, 2 μm). (F) Quantification of TRPV1 fluorescence intensity (n = 10 cells per condition; Student’s t-test, ***p < 0.001). (G) Immunoblot showing TRPV1 expression in WT BMDMs 48 h after transfection with scramble or TRPV1 siRNA. (H-J) Quantification of FBGC formation following TRPV1 knockdown: (H) number of FBGCs per high-power field, (I) percentage of fused BMDMs, and (J) average FBGC size. Data represent n = 3 biological replicates with 5 images per group; Student’s t-test, ***p < 0.001.

    Article Snippet: Primary antibodies comprised anti-actin (cat# 4970S; Cell Signaling Technology, Danvers, MA) and anti-TRPV1 (cat# ACC-030), anti-TRPV2 (cat# ACC-039), and anti-TRPA1 (cat# ACC-037) from Alomone Labs. Species-appropriate secondary antibodies (goat, rabbit, and mouse) were obtained from Jackson ImmunoResearch.

    Techniques: Staining, Immunofluorescence, Transfection, Fluorescence, Western Blot, Expressing, Knockdown