rabbit polyclonal anti p2rx7 extracellular antibody  (Alomone Labs)


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    Structured Review

    Alomone Labs rabbit polyclonal anti p2rx7 extracellular antibody
    <t>P2RX7</t> expression is required for AβOs-induced RPE degeneration. Eyes were treated with a single subretinal injection of 1 μM AβOs. Tissue was collected 7 days after injection. a P2rx7 −/− mice are protected from AβOs-induced RPE degeneration, n = 8. b Lower magnification (left panel) and higher magnification (right panel) of RPE flat mounts of P2rx7 hP2RX7Flox and P2rx7 hP2RX7Flox / Best1-Cre+ mice stained with phalloidin (white) and P2RX7 (yellow) demonstrating reduction of P2RX7 signal in the RPE of P2rx7 hP2RX7Flox / Best1-Cre+ mice compared to P2rx7 hP2RX7Flox mice. Black arrowhead points to the optic nerve of P2rx7 hP2RX7Flox / Best1-Cre+ mice, where expression of P2RX persists in non-RPE tissue. c AβOs induced degeneration in P2rx7 hP2RX7Flox ( n = 6) but not in P2rx7 hP2RX7Flox / Best1-Cre+ mice ( n = 8) ( d ). Representative images are shown. Fundus photographs, top row; Flat mounts stained for zonula occludens-1 (ZO-1; red), bottom row. Degeneration outlined by white arrowheads. Binary (Healthy %) and morphometric (PM, polymegethism (mean (SEM)) quantification of RPE degeneration is shown (Fisher’s exact test for binary; two-tailed t -test for morphometry; * P
    Rabbit Polyclonal Anti P2rx7 Extracellular Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit polyclonal anti p2rx7 extracellular antibody/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
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    rabbit polyclonal anti p2rx7 extracellular antibody - by Bioz Stars, 2022-12
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    Images

    1) Product Images from "Nucleoside reverse transcriptase inhibitors and Kamuvudines inhibit amyloid-β induced retinal pigmented epithelium degeneration"

    Article Title: Nucleoside reverse transcriptase inhibitors and Kamuvudines inhibit amyloid-β induced retinal pigmented epithelium degeneration

    Journal: Signal Transduction and Targeted Therapy

    doi: 10.1038/s41392-021-00537-z

    P2RX7 expression is required for AβOs-induced RPE degeneration. Eyes were treated with a single subretinal injection of 1 μM AβOs. Tissue was collected 7 days after injection. a P2rx7 −/− mice are protected from AβOs-induced RPE degeneration, n = 8. b Lower magnification (left panel) and higher magnification (right panel) of RPE flat mounts of P2rx7 hP2RX7Flox and P2rx7 hP2RX7Flox / Best1-Cre+ mice stained with phalloidin (white) and P2RX7 (yellow) demonstrating reduction of P2RX7 signal in the RPE of P2rx7 hP2RX7Flox / Best1-Cre+ mice compared to P2rx7 hP2RX7Flox mice. Black arrowhead points to the optic nerve of P2rx7 hP2RX7Flox / Best1-Cre+ mice, where expression of P2RX persists in non-RPE tissue. c AβOs induced degeneration in P2rx7 hP2RX7Flox ( n = 6) but not in P2rx7 hP2RX7Flox / Best1-Cre+ mice ( n = 8) ( d ). Representative images are shown. Fundus photographs, top row; Flat mounts stained for zonula occludens-1 (ZO-1; red), bottom row. Degeneration outlined by white arrowheads. Binary (Healthy %) and morphometric (PM, polymegethism (mean (SEM)) quantification of RPE degeneration is shown (Fisher’s exact test for binary; two-tailed t -test for morphometry; * P
    Figure Legend Snippet: P2RX7 expression is required for AβOs-induced RPE degeneration. Eyes were treated with a single subretinal injection of 1 μM AβOs. Tissue was collected 7 days after injection. a P2rx7 −/− mice are protected from AβOs-induced RPE degeneration, n = 8. b Lower magnification (left panel) and higher magnification (right panel) of RPE flat mounts of P2rx7 hP2RX7Flox and P2rx7 hP2RX7Flox / Best1-Cre+ mice stained with phalloidin (white) and P2RX7 (yellow) demonstrating reduction of P2RX7 signal in the RPE of P2rx7 hP2RX7Flox / Best1-Cre+ mice compared to P2rx7 hP2RX7Flox mice. Black arrowhead points to the optic nerve of P2rx7 hP2RX7Flox / Best1-Cre+ mice, where expression of P2RX persists in non-RPE tissue. c AβOs induced degeneration in P2rx7 hP2RX7Flox ( n = 6) but not in P2rx7 hP2RX7Flox / Best1-Cre+ mice ( n = 8) ( d ). Representative images are shown. Fundus photographs, top row; Flat mounts stained for zonula occludens-1 (ZO-1; red), bottom row. Degeneration outlined by white arrowheads. Binary (Healthy %) and morphometric (PM, polymegethism (mean (SEM)) quantification of RPE degeneration is shown (Fisher’s exact test for binary; two-tailed t -test for morphometry; * P

    Techniques Used: Expressing, Injection, Mouse Assay, Staining, Two Tailed Test

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    Alomone Labs anti p2x7 receptor extracellular antibody
    Sciatic nerve conduction velocity. The nerve conduction velocity of the DNP group was significantly lower than that of normal rats; however, there were no differences among the DNP, <t>P2X7</t> shRNA, and NC groups. Intrathecal injection of P2X7 shRNA and p38 inhibitors decreased the rate of nerve injury. Data are shown as mean ± SEM based on at least three independent experiments, n = 6; ** p
    Anti P2x7 Receptor Extracellular Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Price from $9.99 to $1999.99
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    94
    Alomone Labs anti p2x7 receptor extracellular fitc antibody
    Tregs and <t>anti-inflammatory</t> cytokines in <t>P2X7R-regulated</t> acute gouty arthritis. ( A ) The expressions of Tregs among the three groups at 12h. ( B ) The levels of CD4 + CD25 + FOXP3 + Tregs in three groups at each time point. ( C) The expression of FOXP3 mRNA among three groups at each time point. ( D -E) The expressions of TGF-β 1 and IL-10 in serum among the three groups. *P
    Anti P2x7 Receptor Extracellular Fitc Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti p2x7 receptor extracellular fitc antibody/product/Alomone Labs
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    Sciatic nerve conduction velocity. The nerve conduction velocity of the DNP group was significantly lower than that of normal rats; however, there were no differences among the DNP, P2X7 shRNA, and NC groups. Intrathecal injection of P2X7 shRNA and p38 inhibitors decreased the rate of nerve injury. Data are shown as mean ± SEM based on at least three independent experiments, n = 6; ** p

    Journal: International Journal of Molecular Sciences

    Article Title: Silencing P2X7R Alleviates Diabetic Neuropathic Pain Involving TRPV1 via PKCε/P38MAPK/NF-κB Signaling Pathway in Rats

    doi: 10.3390/ijms232214141

    Figure Lengend Snippet: Sciatic nerve conduction velocity. The nerve conduction velocity of the DNP group was significantly lower than that of normal rats; however, there were no differences among the DNP, P2X7 shRNA, and NC groups. Intrathecal injection of P2X7 shRNA and p38 inhibitors decreased the rate of nerve injury. Data are shown as mean ± SEM based on at least three independent experiments, n = 6; ** p

    Article Snippet: P2X7 (APR-008, Alomone, Jerusalem, Israel), 1:800; TRPV1 (Bioss, Beijing, China) 1:1000; p38 (Cell Signaling Technology; CST, Boston, MA, USA), 1:800; phosphor- p38 (CST, Boston, USA), 1:800; PKCε (Proteintech, Hubei, China), 1:800; p65 (CST, Boston, USA), 1:2000; pp65 (CST, Boston, USA), 1:800; IL-1β (Affinity Biosciences, Jiangsu, China), 1:300; TNF-α (Boster, Wuhan, China), 1:500, were to incubate PVDF membranes overnight at 4 °C.

    Techniques: shRNA, Injection

    Measuring TRPV1 mRNA and protein levels and co-expression of NeuN and TRPV1 in DRG. ( A ) TRPV1 mRNA levels in the DRG. ( B ) TRPV1 protein bands in the DRG. ( C ) TRPV1 protein expression in DRG. ( D ) Co-expression of TRPV1 and NeuN in DRG. ( E ) Relative fluorescence intensity levels of NeuN and TRPV1 co-expression. TRPV1 mRNA, protein expression, and the co-expression of NeuN and TRPV1 in the P2X7 shRNA and p38 inhibitor groups were lower than in the DNP group. Blue staining (DAPI) marks the nucleus, green staining (NeuN) marks the neuron, red staining marks TRPV1, and the yellow signal is a combination of green and red signals. The scale bar represents 50 μm; data are shown as mean ± SEM based on at least three independent experiments, n = 6; ** p

    Journal: International Journal of Molecular Sciences

    Article Title: Silencing P2X7R Alleviates Diabetic Neuropathic Pain Involving TRPV1 via PKCε/P38MAPK/NF-κB Signaling Pathway in Rats

    doi: 10.3390/ijms232214141

    Figure Lengend Snippet: Measuring TRPV1 mRNA and protein levels and co-expression of NeuN and TRPV1 in DRG. ( A ) TRPV1 mRNA levels in the DRG. ( B ) TRPV1 protein bands in the DRG. ( C ) TRPV1 protein expression in DRG. ( D ) Co-expression of TRPV1 and NeuN in DRG. ( E ) Relative fluorescence intensity levels of NeuN and TRPV1 co-expression. TRPV1 mRNA, protein expression, and the co-expression of NeuN and TRPV1 in the P2X7 shRNA and p38 inhibitor groups were lower than in the DNP group. Blue staining (DAPI) marks the nucleus, green staining (NeuN) marks the neuron, red staining marks TRPV1, and the yellow signal is a combination of green and red signals. The scale bar represents 50 μm; data are shown as mean ± SEM based on at least three independent experiments, n = 6; ** p

    Article Snippet: P2X7 (APR-008, Alomone, Jerusalem, Israel), 1:800; TRPV1 (Bioss, Beijing, China) 1:1000; p38 (Cell Signaling Technology; CST, Boston, MA, USA), 1:800; phosphor- p38 (CST, Boston, USA), 1:800; PKCε (Proteintech, Hubei, China), 1:800; p65 (CST, Boston, USA), 1:2000; pp65 (CST, Boston, USA), 1:800; IL-1β (Affinity Biosciences, Jiangsu, China), 1:300; TNF-α (Boster, Wuhan, China), 1:500, were to incubate PVDF membranes overnight at 4 °C.

    Techniques: Expressing, Fluorescence, shRNA, Staining

    Results of MWT and TWL of all groups. ( A ) Changes in MWT values. ( B ) Changes in TWL values. At the end of the seventh week, MWT and TWL in the P2X7 shRNA and p38 inhibitor groups were higher than in the DNP group. The X-axis means the time of measuring behavior and drug administration, the detailed descriptions of 0, 1, 5, 6 and 7 are given in the Section 4 ; data are shown as mean ± SEM based on at least three independent experiments, n = 6; ** p

    Journal: International Journal of Molecular Sciences

    Article Title: Silencing P2X7R Alleviates Diabetic Neuropathic Pain Involving TRPV1 via PKCε/P38MAPK/NF-κB Signaling Pathway in Rats

    doi: 10.3390/ijms232214141

    Figure Lengend Snippet: Results of MWT and TWL of all groups. ( A ) Changes in MWT values. ( B ) Changes in TWL values. At the end of the seventh week, MWT and TWL in the P2X7 shRNA and p38 inhibitor groups were higher than in the DNP group. The X-axis means the time of measuring behavior and drug administration, the detailed descriptions of 0, 1, 5, 6 and 7 are given in the Section 4 ; data are shown as mean ± SEM based on at least three independent experiments, n = 6; ** p

    Article Snippet: P2X7 (APR-008, Alomone, Jerusalem, Israel), 1:800; TRPV1 (Bioss, Beijing, China) 1:1000; p38 (Cell Signaling Technology; CST, Boston, MA, USA), 1:800; phosphor- p38 (CST, Boston, USA), 1:800; PKCε (Proteintech, Hubei, China), 1:800; p65 (CST, Boston, USA), 1:2000; pp65 (CST, Boston, USA), 1:800; IL-1β (Affinity Biosciences, Jiangsu, China), 1:300; TNF-α (Boster, Wuhan, China), 1:500, were to incubate PVDF membranes overnight at 4 °C.

    Techniques: shRNA

    Measurement of P2X7 mRNA and protein levels in the DRG and co-expression levels of P2X7R with GFAP. ( A ) P2X7 mRNA. ( B ) SDS-PAGE of P2X7R protein in DRG of experimental rats in each group. ( C ) P2X7R protein expression in the DRG of each group was analyzed. ( D ) Co-expression of GFAP and P2X7R in DRG. ( E ) Relative fluorescence intensity levels of GFAP in each group. ( F ) Relative fluorescence intensity levels of GFAP and P2X7R co-expression. P2X7 mRNA, protein levels, and co-expression levels of P2X7R and GFAP in the P2X7 shRNA group were lower than in the DNP rats. Blue staining (DAPI) marks the nucleus, green staining (GFAP) marks activated SGCs, and red staining marks P2X7R. The scale bar represents 50 µm; data are shown as mean ± SEM based on at least three independent experiments, n = 6; ** p

    Journal: International Journal of Molecular Sciences

    Article Title: Silencing P2X7R Alleviates Diabetic Neuropathic Pain Involving TRPV1 via PKCε/P38MAPK/NF-κB Signaling Pathway in Rats

    doi: 10.3390/ijms232214141

    Figure Lengend Snippet: Measurement of P2X7 mRNA and protein levels in the DRG and co-expression levels of P2X7R with GFAP. ( A ) P2X7 mRNA. ( B ) SDS-PAGE of P2X7R protein in DRG of experimental rats in each group. ( C ) P2X7R protein expression in the DRG of each group was analyzed. ( D ) Co-expression of GFAP and P2X7R in DRG. ( E ) Relative fluorescence intensity levels of GFAP in each group. ( F ) Relative fluorescence intensity levels of GFAP and P2X7R co-expression. P2X7 mRNA, protein levels, and co-expression levels of P2X7R and GFAP in the P2X7 shRNA group were lower than in the DNP rats. Blue staining (DAPI) marks the nucleus, green staining (GFAP) marks activated SGCs, and red staining marks P2X7R. The scale bar represents 50 µm; data are shown as mean ± SEM based on at least three independent experiments, n = 6; ** p

    Article Snippet: P2X7 (APR-008, Alomone, Jerusalem, Israel), 1:800; TRPV1 (Bioss, Beijing, China) 1:1000; p38 (Cell Signaling Technology; CST, Boston, MA, USA), 1:800; phosphor- p38 (CST, Boston, USA), 1:800; PKCε (Proteintech, Hubei, China), 1:800; p65 (CST, Boston, USA), 1:2000; pp65 (CST, Boston, USA), 1:800; IL-1β (Affinity Biosciences, Jiangsu, China), 1:300; TNF-α (Boster, Wuhan, China), 1:500, were to incubate PVDF membranes overnight at 4 °C.

    Techniques: Expressing, SDS Page, Fluorescence, shRNA, Staining

    QSG inhibited the P2X7R-NEK7-NLRP3 inflammasome pathway. ( A ) Determination of potassium ion concentration in RAW264.7 macrophages supernatant. ( B ) The effective concentration range of CCK8 to detect AZ. ( C ) Representative graph of optimal concentration of AZ for WB validation. ( D ) Representative immunofluorescence detection images of RAW264.7 macrophages P2X7R expression. Scale bar=25 µm. ( E – H ) Western blot analysis showed that both QSG and AZ treatment reduced the expression of P2X7R, Caspase-1, IL-18, IL-1β in RAW264.7 macrophages, N = 3 per group. ### P

    Journal: Journal of Inflammation Research

    Article Title: P2X7R-NEK7-NLRP3 Inflammasome Activation: A Novel Therapeutic Pathway of Qishen Granule in the Treatment of Acute Myocardial Ischemia

    doi: 10.2147/JIR.S373962

    Figure Lengend Snippet: QSG inhibited the P2X7R-NEK7-NLRP3 inflammasome pathway. ( A ) Determination of potassium ion concentration in RAW264.7 macrophages supernatant. ( B ) The effective concentration range of CCK8 to detect AZ. ( C ) Representative graph of optimal concentration of AZ for WB validation. ( D ) Representative immunofluorescence detection images of RAW264.7 macrophages P2X7R expression. Scale bar=25 µm. ( E – H ) Western blot analysis showed that both QSG and AZ treatment reduced the expression of P2X7R, Caspase-1, IL-18, IL-1β in RAW264.7 macrophages, N = 3 per group. ### P

    Article Snippet: The primary antibodies used are as follows: anti-Caspase-1 antibody (ab1872, Abcam, USA), anti-P2X7R antibody (APR-008, Alomone, Israel).

    Techniques: Concentration Assay, Western Blot, Immunofluorescence, Expressing

    QSG inhibited LPS combined with ATP-induced NLRP3 inflammasome activation in RAW264.7 macrophages. ( A ) Establishment of LPS combined with ATP to induce NLRP3 inflammasome activation model. ( B ) Immunofluorescence determined that LPS in combination with ATP activates NLRP3 inflammasome. Scale bar=75 µm. ( C ) Safe concentration of QSG in RAW264.7 macrophages. ( D ) Experimental protocol for QSG in LPS combined with ATP to induce NLRP3 inflammasome activation in RAW264.7 macrophages. ( E ) Effective concentration of QSG in RAW264.7 macrophages. ( F ) MCC950 inhibitor concentration range in RAW264.7 macrophages. ( G – M ) Western blot analysis showed that QSG treatment reduced the expression of P2X7R, NEK7, NLRP3, ASC, Caspase-1, IL-18, IL-1β in RAW264.7 macrophages. N = 3 per group. ## P

    Journal: Journal of Inflammation Research

    Article Title: P2X7R-NEK7-NLRP3 Inflammasome Activation: A Novel Therapeutic Pathway of Qishen Granule in the Treatment of Acute Myocardial Ischemia

    doi: 10.2147/JIR.S373962

    Figure Lengend Snippet: QSG inhibited LPS combined with ATP-induced NLRP3 inflammasome activation in RAW264.7 macrophages. ( A ) Establishment of LPS combined with ATP to induce NLRP3 inflammasome activation model. ( B ) Immunofluorescence determined that LPS in combination with ATP activates NLRP3 inflammasome. Scale bar=75 µm. ( C ) Safe concentration of QSG in RAW264.7 macrophages. ( D ) Experimental protocol for QSG in LPS combined with ATP to induce NLRP3 inflammasome activation in RAW264.7 macrophages. ( E ) Effective concentration of QSG in RAW264.7 macrophages. ( F ) MCC950 inhibitor concentration range in RAW264.7 macrophages. ( G – M ) Western blot analysis showed that QSG treatment reduced the expression of P2X7R, NEK7, NLRP3, ASC, Caspase-1, IL-18, IL-1β in RAW264.7 macrophages. N = 3 per group. ## P

    Article Snippet: The primary antibodies used are as follows: anti-Caspase-1 antibody (ab1872, Abcam, USA), anti-P2X7R antibody (APR-008, Alomone, Israel).

    Techniques: Activation Assay, Immunofluorescence, Concentration Assay, Western Blot, Expressing

    QSG inhibited NLRP3 inflamat some activation in cardiac tissue macrophages. ( A ) Representative NLRP3/ASC/Caspase-1 immunofluorescent staining images of AMI mice in each group. Scale bar=20 µm. ( B ) Representative CD86/Caspase-1 immunofluorescent staining images of AMI mice in each group. Scale bar=20 µm. ( C – I ) Western blot analysis showed that QSG treatment reduced the expression of P2X7R, NEK7, NLRP3, ASC, Caspase-1, IL-18, IL-1β in cardiac tissue macrophages. Proteins had been normalized to GAPDH, N = 6 per group. ### P

    Journal: Journal of Inflammation Research

    Article Title: P2X7R-NEK7-NLRP3 Inflammasome Activation: A Novel Therapeutic Pathway of Qishen Granule in the Treatment of Acute Myocardial Ischemia

    doi: 10.2147/JIR.S373962

    Figure Lengend Snippet: QSG inhibited NLRP3 inflamat some activation in cardiac tissue macrophages. ( A ) Representative NLRP3/ASC/Caspase-1 immunofluorescent staining images of AMI mice in each group. Scale bar=20 µm. ( B ) Representative CD86/Caspase-1 immunofluorescent staining images of AMI mice in each group. Scale bar=20 µm. ( C – I ) Western blot analysis showed that QSG treatment reduced the expression of P2X7R, NEK7, NLRP3, ASC, Caspase-1, IL-18, IL-1β in cardiac tissue macrophages. Proteins had been normalized to GAPDH, N = 6 per group. ### P

    Article Snippet: The primary antibodies used are as follows: anti-Caspase-1 antibody (ab1872, Abcam, USA), anti-P2X7R antibody (APR-008, Alomone, Israel).

    Techniques: Activation Assay, Staining, Mouse Assay, Western Blot, Expressing

    QSG might protect AMI through the P2X7R-NEK7-NLRP3 pathway.

    Journal: Journal of Inflammation Research

    Article Title: P2X7R-NEK7-NLRP3 Inflammasome Activation: A Novel Therapeutic Pathway of Qishen Granule in the Treatment of Acute Myocardial Ischemia

    doi: 10.2147/JIR.S373962

    Figure Lengend Snippet: QSG might protect AMI through the P2X7R-NEK7-NLRP3 pathway.

    Article Snippet: The primary antibodies used are as follows: anti-Caspase-1 antibody (ab1872, Abcam, USA), anti-P2X7R antibody (APR-008, Alomone, Israel).

    Techniques:

    QSG regulates the P2X7R-NEK7-NLRP3 pathway. ( A ) mP2X7R pcDNA3.1–3xFlag-T2A-EGFP map. ( B ) WB images of images of RAW264.7 macrophages and analysis of P2X7R. ( C ) Representative immunofluorescence detection images of Caspase-1. Scale bar=75 µm. ( D and E ) Western blot images of RAW264.7 macrophages and analysis of IL-18 and IL-1β. ( F – H ) RAW264.7 macrophages were transfected with P2X7R pcDNA3.1 followed by immunoprecipitation and immunoblot using NEK7 antibody to analyze the protein expression levels of NEK7, NLRP3. The Input represents total protein extracts used for immunoprecipitation. GAPDH was used as a loading control. IB, immunoblot. IP, immunoprecipitation. IgG, negative control. ### P

    Journal: Journal of Inflammation Research

    Article Title: P2X7R-NEK7-NLRP3 Inflammasome Activation: A Novel Therapeutic Pathway of Qishen Granule in the Treatment of Acute Myocardial Ischemia

    doi: 10.2147/JIR.S373962

    Figure Lengend Snippet: QSG regulates the P2X7R-NEK7-NLRP3 pathway. ( A ) mP2X7R pcDNA3.1–3xFlag-T2A-EGFP map. ( B ) WB images of images of RAW264.7 macrophages and analysis of P2X7R. ( C ) Representative immunofluorescence detection images of Caspase-1. Scale bar=75 µm. ( D and E ) Western blot images of RAW264.7 macrophages and analysis of IL-18 and IL-1β. ( F – H ) RAW264.7 macrophages were transfected with P2X7R pcDNA3.1 followed by immunoprecipitation and immunoblot using NEK7 antibody to analyze the protein expression levels of NEK7, NLRP3. The Input represents total protein extracts used for immunoprecipitation. GAPDH was used as a loading control. IB, immunoblot. IP, immunoprecipitation. IgG, negative control. ### P

    Article Snippet: The primary antibodies used are as follows: anti-Caspase-1 antibody (ab1872, Abcam, USA), anti-P2X7R antibody (APR-008, Alomone, Israel).

    Techniques: Western Blot, Immunofluorescence, Transfection, Immunoprecipitation, Expressing, Negative Control

    Tregs and anti-inflammatory cytokines in P2X7R-regulated acute gouty arthritis. ( A ) The expressions of Tregs among the three groups at 12h. ( B ) The levels of CD4 + CD25 + FOXP3 + Tregs in three groups at each time point. ( C) The expression of FOXP3 mRNA among three groups at each time point. ( D -E) The expressions of TGF-β 1 and IL-10 in serum among the three groups. *P

    Journal: Journal of Inflammation Research

    Article Title: ATP-Activated P2X7R Promote the Attack of Acute Gouty Arthritis in Rats Through Activating NLRP3 Inflammasome and Inflammatory Cytokine Production

    doi: 10.2147/JIR.S351660

    Figure Lengend Snippet: Tregs and anti-inflammatory cytokines in P2X7R-regulated acute gouty arthritis. ( A ) The expressions of Tregs among the three groups at 12h. ( B ) The levels of CD4 + CD25 + FOXP3 + Tregs in three groups at each time point. ( C) The expression of FOXP3 mRNA among three groups at each time point. ( D -E) The expressions of TGF-β 1 and IL-10 in serum among the three groups. *P

    Article Snippet: The treated spleen cells (1×10^6cells) were stained with anti-P2X7 receptor (extracellular)-FITC antibody (Alomone, Jerusalem, Israel) and CD68 antibody (NOVUS, Littleton, USA), and the white cell suspension obtained from the spleen was stained with FITC conjugated mouse anti-rat CD4, PE conjugated mouse anti-rat CD25 (BD Bioscience, MD, USA), PE conjugated anti-IL-17A and APC conjugated anti-Foxp3 antibodies (eBioscience, San Jose, CA, USA).

    Techniques: Expressing

    P2X7R regulates the development of acute gouty arthritis in rats. ( A ) At 12h, clinical manifestations of right ankle joint in rats among ATP group, BBG group and control group. ( B and C ) Clinical score and swelling index of three groups of rats at each time point. ( D ) Inflammatory cells infiltrated the synovial tissue of the right ankle joint in three groups of rats, at 24h. ( E and F ) Infiltration of mononuclear cells and neutrophils in the synovial tissue of the ankle joint among the three groups. * P

    Journal: Journal of Inflammation Research

    Article Title: ATP-Activated P2X7R Promote the Attack of Acute Gouty Arthritis in Rats Through Activating NLRP3 Inflammasome and Inflammatory Cytokine Production

    doi: 10.2147/JIR.S351660

    Figure Lengend Snippet: P2X7R regulates the development of acute gouty arthritis in rats. ( A ) At 12h, clinical manifestations of right ankle joint in rats among ATP group, BBG group and control group. ( B and C ) Clinical score and swelling index of three groups of rats at each time point. ( D ) Inflammatory cells infiltrated the synovial tissue of the right ankle joint in three groups of rats, at 24h. ( E and F ) Infiltration of mononuclear cells and neutrophils in the synovial tissue of the ankle joint among the three groups. * P

    Article Snippet: The treated spleen cells (1×10^6cells) were stained with anti-P2X7 receptor (extracellular)-FITC antibody (Alomone, Jerusalem, Israel) and CD68 antibody (NOVUS, Littleton, USA), and the white cell suspension obtained from the spleen was stained with FITC conjugated mouse anti-rat CD4, PE conjugated mouse anti-rat CD25 (BD Bioscience, MD, USA), PE conjugated anti-IL-17A and APC conjugated anti-Foxp3 antibodies (eBioscience, San Jose, CA, USA).

    Techniques:

    P2X7R promote Th17 cells and pro-inflammatory cytokines production. ( A ) The expressions of CD4 + IL-17 + Th17 cells among the three groups at 12h. ( B ) The levels of CD4 + IL-17 + Th17 cells in ATP group, BBG group and Control group at each time point. ( C-E ) The serum levels of IL-1β, IL-6 and IL-17 of the three groups at each time point. (F) The expression of IL-17 mRNA among three groups at each time point. * P

    Journal: Journal of Inflammation Research

    Article Title: ATP-Activated P2X7R Promote the Attack of Acute Gouty Arthritis in Rats Through Activating NLRP3 Inflammasome and Inflammatory Cytokine Production

    doi: 10.2147/JIR.S351660

    Figure Lengend Snippet: P2X7R promote Th17 cells and pro-inflammatory cytokines production. ( A ) The expressions of CD4 + IL-17 + Th17 cells among the three groups at 12h. ( B ) The levels of CD4 + IL-17 + Th17 cells in ATP group, BBG group and Control group at each time point. ( C-E ) The serum levels of IL-1β, IL-6 and IL-17 of the three groups at each time point. (F) The expression of IL-17 mRNA among three groups at each time point. * P

    Article Snippet: The treated spleen cells (1×10^6cells) were stained with anti-P2X7 receptor (extracellular)-FITC antibody (Alomone, Jerusalem, Israel) and CD68 antibody (NOVUS, Littleton, USA), and the white cell suspension obtained from the spleen was stained with FITC conjugated mouse anti-rat CD4, PE conjugated mouse anti-rat CD25 (BD Bioscience, MD, USA), PE conjugated anti-IL-17A and APC conjugated anti-Foxp3 antibodies (eBioscience, San Jose, CA, USA).

    Techniques: Expressing

    P2X7R mediated NLRP3 inflammatory-dependent IL-1β secretion on macrophages. The expressions of P2X7R ( A ), NLRP3 ( B ) and IL-1β ( C ) in rat spleen macrophages were analyzed by qRT-PCR. *P

    Journal: Journal of Inflammation Research

    Article Title: ATP-Activated P2X7R Promote the Attack of Acute Gouty Arthritis in Rats Through Activating NLRP3 Inflammasome and Inflammatory Cytokine Production

    doi: 10.2147/JIR.S351660

    Figure Lengend Snippet: P2X7R mediated NLRP3 inflammatory-dependent IL-1β secretion on macrophages. The expressions of P2X7R ( A ), NLRP3 ( B ) and IL-1β ( C ) in rat spleen macrophages were analyzed by qRT-PCR. *P

    Article Snippet: The treated spleen cells (1×10^6cells) were stained with anti-P2X7 receptor (extracellular)-FITC antibody (Alomone, Jerusalem, Israel) and CD68 antibody (NOVUS, Littleton, USA), and the white cell suspension obtained from the spleen was stained with FITC conjugated mouse anti-rat CD4, PE conjugated mouse anti-rat CD25 (BD Bioscience, MD, USA), PE conjugated anti-IL-17A and APC conjugated anti-Foxp3 antibodies (eBioscience, San Jose, CA, USA).

    Techniques: Quantitative RT-PCR

    The expression changes of P2X7R on macrophages affect their ability to take up YO-PRO-1. ( A ) At 12h, the expression level of P2X7R in each group of macrophages was detected by flow cytometry. ( B ) Expression of P2X7R among the three groups at different time points. ( C ) At 12h, the percentage of YO-PRO-1 uptake by macrophages in each group was detected by flow cytometry. ( D ) The ability of macrophages to uptake YO-PRO-1 among the three groups at each time point. ( E ) The expression level of P2X7R was positively correlated with the ability of macrophages to uptake YO-PRO-1. * P

    Journal: Journal of Inflammation Research

    Article Title: ATP-Activated P2X7R Promote the Attack of Acute Gouty Arthritis in Rats Through Activating NLRP3 Inflammasome and Inflammatory Cytokine Production

    doi: 10.2147/JIR.S351660

    Figure Lengend Snippet: The expression changes of P2X7R on macrophages affect their ability to take up YO-PRO-1. ( A ) At 12h, the expression level of P2X7R in each group of macrophages was detected by flow cytometry. ( B ) Expression of P2X7R among the three groups at different time points. ( C ) At 12h, the percentage of YO-PRO-1 uptake by macrophages in each group was detected by flow cytometry. ( D ) The ability of macrophages to uptake YO-PRO-1 among the three groups at each time point. ( E ) The expression level of P2X7R was positively correlated with the ability of macrophages to uptake YO-PRO-1. * P

    Article Snippet: The treated spleen cells (1×10^6cells) were stained with anti-P2X7 receptor (extracellular)-FITC antibody (Alomone, Jerusalem, Israel) and CD68 antibody (NOVUS, Littleton, USA), and the white cell suspension obtained from the spleen was stained with FITC conjugated mouse anti-rat CD4, PE conjugated mouse anti-rat CD25 (BD Bioscience, MD, USA), PE conjugated anti-IL-17A and APC conjugated anti-Foxp3 antibodies (eBioscience, San Jose, CA, USA).

    Techniques: Expressing, Flow Cytometry

    The changing trend of cytokines and Treg/Th17 cells matched with the pathogenesis process of ATP-activated P2X7R-regulated acute gouty arthritis. ( A ) The trends of P2X7R and IL-1β in ATP group. ( B ) The trends of CD4 + IL-17 + Th17 cells and IL-17 in ATP group. ( C ) The trends of CD4 + CD25 + Foxp3 + Treg cells and TGF-β 1 in ATP group. ( D ) The trends of CD4 + CD25 + Foxp3 + Treg cells and CD4 + IL-17 + Th17 cells in ATP group. ( E ) The ratios of Treg/Th17 among ATP group, BBG group and Control group. * P

    Journal: Journal of Inflammation Research

    Article Title: ATP-Activated P2X7R Promote the Attack of Acute Gouty Arthritis in Rats Through Activating NLRP3 Inflammasome and Inflammatory Cytokine Production

    doi: 10.2147/JIR.S351660

    Figure Lengend Snippet: The changing trend of cytokines and Treg/Th17 cells matched with the pathogenesis process of ATP-activated P2X7R-regulated acute gouty arthritis. ( A ) The trends of P2X7R and IL-1β in ATP group. ( B ) The trends of CD4 + IL-17 + Th17 cells and IL-17 in ATP group. ( C ) The trends of CD4 + CD25 + Foxp3 + Treg cells and TGF-β 1 in ATP group. ( D ) The trends of CD4 + CD25 + Foxp3 + Treg cells and CD4 + IL-17 + Th17 cells in ATP group. ( E ) The ratios of Treg/Th17 among ATP group, BBG group and Control group. * P

    Article Snippet: The treated spleen cells (1×10^6cells) were stained with anti-P2X7 receptor (extracellular)-FITC antibody (Alomone, Jerusalem, Israel) and CD68 antibody (NOVUS, Littleton, USA), and the white cell suspension obtained from the spleen was stained with FITC conjugated mouse anti-rat CD4, PE conjugated mouse anti-rat CD25 (BD Bioscience, MD, USA), PE conjugated anti-IL-17A and APC conjugated anti-Foxp3 antibodies (eBioscience, San Jose, CA, USA).

    Techniques: