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Cell Signaling Technology Inc il 1β
Il 1β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 989 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/il 1β/product/Cell Signaling Technology Inc
Average 97 stars, based on 989 article reviews

il 1β - by Bioz Stars, 2026-06

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TMH inhibits activation of the NLRP3 inflammasome. (A) Schematic workflow of in vitro NLRP3 inflammasome activation. (B,C) Cell viability was assessed in J774A.1 cells (B) and PMA (500 nM)-differentiated THP-1 cells (C) treated with TMH for 2 or 18 h using the EZ-Cytox assay. (D) LPS-primed J774A.1 cells were treated with TMH for 2 h, then stimulated with ATP (5 mM) for 30 min in the presence or absence of MCC950. IL-1β (p17) levels in supernatants were measured by ELISA. (E,F) PMA-differentiated THP-1 cells were primed with LPS, treated with TMH for 2 h, then stimulated with ATP (5 mM) (E) or nigericin (10 μM) (F) for 1 h, with or without MCC950. IL-1β (p17) levels in supernatants were determined by ELISA. Data are presented as the mean ± SD (n = 3). Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparisons test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001; n.s., not significant.

Journal: Frontiers in Pharmacology

Article Title: Thymelaea hirsuta (L.) Endl . extract attenuates NLRP3 inflammasome activation via modulation of ATPase activity

doi: 10.3389/fphar.2026.1781860

Figure Lengend Snippet: TMH inhibits activation of the NLRP3 inflammasome. (A) Schematic workflow of in vitro NLRP3 inflammasome activation. (B,C) Cell viability was assessed in J774A.1 cells (B) and PMA (500 nM)-differentiated THP-1 cells (C) treated with TMH for 2 or 18 h using the EZ-Cytox assay. (D) LPS-primed J774A.1 cells were treated with TMH for 2 h, then stimulated with ATP (5 mM) for 30 min in the presence or absence of MCC950. IL-1β (p17) levels in supernatants were measured by ELISA. (E,F) PMA-differentiated THP-1 cells were primed with LPS, treated with TMH for 2 h, then stimulated with ATP (5 mM) (E) or nigericin (10 μM) (F) for 1 h, with or without MCC950. IL-1β (p17) levels in supernatants were determined by ELISA. Data are presented as the mean ± SD (n = 3). Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparisons test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001; n.s., not significant.

Article Snippet: Antibodies specific for human IL-1β (AF-401-NA) and mouse IL-1β (AF-201-NA) were purchased from R&D Systems (United States).

Techniques: Activation Assay, In Vitro, Enzyme-linked Immunosorbent Assay

$TMH does not affect other inflammasome or inflammatory pathways. (A,B) LPS-primed J774A.1 cells were treated with TMH for 2 h, followed by stimulation with either dsDNA (1 μg/mL) (A) or flagellin (B) transfected using Lipofectamine 2000 for 3 h. (C) Following TMH treatment (2 h), nuclear and cytosolic fractions of LPS-primed J774A.1 cells were separated and assessed for NF-κB p65 translocation by immunoblotting. (D) HEK293FT cells transfected with the pGL4.32 luciferase reporter vector were treated with TNF-α (20 ng/mL) for 5 h, with or without TMH pre-treatment (2 h). Luciferase activity was measured using the Bright-Glo™ luciferase assay system (Promega). Data are presented as the mean ± SD (n = 3). Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparisons test n.s., not significant.$

Journal: Frontiers in Pharmacology

Article Title: Thymelaea hirsuta (L.) Endl . extract attenuates NLRP3 inflammasome activation via modulation of ATPase activity

doi: 10.3389/fphar.2026.1781860

Figure Lengend Snippet: TMH does not affect other inflammasome or inflammatory pathways. (A,B) LPS-primed J774A.1 cells were treated with TMH for 2 h, followed by stimulation with either dsDNA (1 μg/mL) (A) or flagellin (B) transfected using Lipofectamine 2000 for 3 h. (C) Following TMH treatment (2 h), nuclear and cytosolic fractions of LPS-primed J774A.1 cells were separated and assessed for NF-κB p65 translocation by immunoblotting. (D) HEK293FT cells transfected with the pGL4.32 luciferase reporter vector were treated with TNF-α (20 ng/mL) for 5 h, with or without TMH pre-treatment (2 h). Luciferase activity was measured using the Bright-Glo™ luciferase assay system (Promega). Data are presented as the mean ± SD (n = 3). Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparisons test n.s., not significant.

Article Snippet: Antibodies specific for human IL-1β (AF-401-NA) and mouse IL-1β (AF-201-NA) were purchased from R&D Systems (United States).

Techniques: Transfection, Translocation Assay, Western Blot, Luciferase, Plasmid Preparation, Activity Assay

TMH inhibits NLRP3 inflammasome activation by suppressing ASC oligomerization and ATPase activity. (A) LPS-primed J774A.1 cells were treated with TMH for 2 h, then stimulated with imiquimod (200 μM) for 1 h. (B) Cells were treated with TMH (2 h), stained with MitoSOX (5 μM, 10 min), and stimulated with ATP (5 mM, 5 min). Intracellular ROS were visualized by confocal microscopy. (C,D) PMA-differentiated THP-1 cells were primed with LPS, treated with TMH for 2 h, then stimulated with nigericin (10 μM, 1 h). ASC speck formation was examined by confocal microscopy (C) , and representative images from five fields are shown (D) . (E) Cells were stimulated with or without MCC950 and cross-linked with DSS (2.5 mM, 30 min) before immunoblotting for ASC oligomerization. (F) NLRP3 ATPase activity was measured using the ADP-Glo™ assay to quantify ATP-to-ADP conversion following TMH treatment. Data are presented as the mean ± SD (n = 3). Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparisons test. **P < 0.01, ***P < 0.001.

Journal: Frontiers in Pharmacology

Article Title: Thymelaea hirsuta (L.) Endl . extract attenuates NLRP3 inflammasome activation via modulation of ATPase activity

doi: 10.3389/fphar.2026.1781860

Figure Lengend Snippet: TMH inhibits NLRP3 inflammasome activation by suppressing ASC oligomerization and ATPase activity. (A) LPS-primed J774A.1 cells were treated with TMH for 2 h, then stimulated with imiquimod (200 μM) for 1 h. (B) Cells were treated with TMH (2 h), stained with MitoSOX (5 μM, 10 min), and stimulated with ATP (5 mM, 5 min). Intracellular ROS were visualized by confocal microscopy. (C,D) PMA-differentiated THP-1 cells were primed with LPS, treated with TMH for 2 h, then stimulated with nigericin (10 μM, 1 h). ASC speck formation was examined by confocal microscopy (C) , and representative images from five fields are shown (D) . (E) Cells were stimulated with or without MCC950 and cross-linked with DSS (2.5 mM, 30 min) before immunoblotting for ASC oligomerization. (F) NLRP3 ATPase activity was measured using the ADP-Glo™ assay to quantify ATP-to-ADP conversion following TMH treatment. Data are presented as the mean ± SD (n = 3). Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparisons test. **P < 0.01, ***P < 0.001.

Article Snippet: Antibodies specific for human IL-1β (AF-401-NA) and mouse IL-1β (AF-201-NA) were purchased from R&D Systems (United States).

Techniques: Activation Assay, Activity Assay, Staining, Confocal Microscopy, Western Blot, Glo Assay

Toxicity assessment of TMH in zebrafish embryos. (A) Survival curves of zebrafish embryos treated with TMH at concentrations of 1, 10, or 100 μg/mL. Sixty embryos were used per condition and maintained in E3 medium. The control group was treated with DMSO (0.25%, v/v), corresponding to the highest TMH concentration. (B) Survival and phenotype distribution of 5 dpf embryos treated with TMH at distinct concentrations from 1 to 5 dpf. (C) Representative images showing developmental abnormalities observed in embryos treated with 10 μg/mL TMH at 5 dpf. (D) Representative images of Sudan Black B staining in 3 dpf embryos treated with vehicle control (0.0025% DMSO with PTU; upper panel) or TMH (1 μg/mL; lower panel). (E) Quantification of neutrophil counts in the CHT (red dashed outline) following treatment with TMH (1 μg/mL). Data are presented as mean ± SEM of individual embryos. Statistical significance was determined using an unpaired two-tailed Student’s t-test; n.s., not significant (p = 0.9997). Scale bars, 300 µm.

Journal: Frontiers in Pharmacology

Article Title: Thymelaea hirsuta (L.) Endl . extract attenuates NLRP3 inflammasome activation via modulation of ATPase activity

doi: 10.3389/fphar.2026.1781860

Figure Lengend Snippet: Toxicity assessment of TMH in zebrafish embryos. (A) Survival curves of zebrafish embryos treated with TMH at concentrations of 1, 10, or 100 μg/mL. Sixty embryos were used per condition and maintained in E3 medium. The control group was treated with DMSO (0.25%, v/v), corresponding to the highest TMH concentration. (B) Survival and phenotype distribution of 5 dpf embryos treated with TMH at distinct concentrations from 1 to 5 dpf. (C) Representative images showing developmental abnormalities observed in embryos treated with 10 μg/mL TMH at 5 dpf. (D) Representative images of Sudan Black B staining in 3 dpf embryos treated with vehicle control (0.0025% DMSO with PTU; upper panel) or TMH (1 μg/mL; lower panel). (E) Quantification of neutrophil counts in the CHT (red dashed outline) following treatment with TMH (1 μg/mL). Data are presented as mean ± SEM of individual embryos. Statistical significance was determined using an unpaired two-tailed Student’s t-test; n.s., not significant (p = 0.9997). Scale bars, 300 µm.

Article Snippet: Antibodies specific for human IL-1β (AF-401-NA) and mouse IL-1β (AF-201-NA) were purchased from R&D Systems (United States).

Techniques: Control, Concentration Assay, Staining, Two Tailed Test

TMH suppresses LPS-induced inflammatory cell recruitment in zebrafish embryos. (A) Representative images of neutrophil recruitment in the CHT in 3 dpf zebrafish embryos following LPS stimulation, assessed by Sudan Black B staining. Top panel: control embryos treated with 0.0025% DMSO (n = 29); middle panel: LPS-treated embryos (10 μg/mL; n = 32); bottom panel: embryos co-treated with LPS (10 μg/mL) and TMH (1 μg/mL; n = 33). (B) Quantification of neutrophil accumulation in the CHT following LPS stimulation with or without TMH treatment using Sudan Black B staining from (A) . (C) Representative images of whole-mount in situ hybridization showing mpx -positive neutrophils in 3 dpf embryos under LPS and TMH treatment conditions. Top panel (DMSO 0.0025%; n = 34); middle panel (LPS 10 μg/mL; n = 35); bottom panel (LPS 10 μg/mL with TMH 1 μg/mL; n = 39). (D) Quantification of mpx -positive cells within the CHT from (C) . (E) Representative confocal images of macrophages in 3 dpf Tg ( mpeg1 :EGFP) zebrafish embryos following LPS and TMH treatment. Top panel (DMSO 0.0025%; n = 8); middle panel (LPS 10 μg/mL; n = 11); bottom panel (LPS 10 μg/mL with TMH 1 μg/mL; n = 13). (F) Quantification of mpeg1 :EGFP-positive macrophages in the CHT region shown in (E) . Red dashed outline indicates the CHT. All data are presented as mean ± SEM. Statistical significance was determined using an unpaired two-tailed Student’s t-test. *P < 0.05; **P < 0.01; ***P < 0.05; ****P < 0.0001. Scale bars, 300 µm.

Journal: Frontiers in Pharmacology

Article Title: Thymelaea hirsuta (L.) Endl . extract attenuates NLRP3 inflammasome activation via modulation of ATPase activity

doi: 10.3389/fphar.2026.1781860

Figure Lengend Snippet: TMH suppresses LPS-induced inflammatory cell recruitment in zebrafish embryos. (A) Representative images of neutrophil recruitment in the CHT in 3 dpf zebrafish embryos following LPS stimulation, assessed by Sudan Black B staining. Top panel: control embryos treated with 0.0025% DMSO (n = 29); middle panel: LPS-treated embryos (10 μg/mL; n = 32); bottom panel: embryos co-treated with LPS (10 μg/mL) and TMH (1 μg/mL; n = 33). (B) Quantification of neutrophil accumulation in the CHT following LPS stimulation with or without TMH treatment using Sudan Black B staining from (A) . (C) Representative images of whole-mount in situ hybridization showing mpx -positive neutrophils in 3 dpf embryos under LPS and TMH treatment conditions. Top panel (DMSO 0.0025%; n = 34); middle panel (LPS 10 μg/mL; n = 35); bottom panel (LPS 10 μg/mL with TMH 1 μg/mL; n = 39). (D) Quantification of mpx -positive cells within the CHT from (C) . (E) Representative confocal images of macrophages in 3 dpf Tg ( mpeg1 :EGFP) zebrafish embryos following LPS and TMH treatment. Top panel (DMSO 0.0025%; n = 8); middle panel (LPS 10 μg/mL; n = 11); bottom panel (LPS 10 μg/mL with TMH 1 μg/mL; n = 13). (F) Quantification of mpeg1 :EGFP-positive macrophages in the CHT region shown in (E) . Red dashed outline indicates the CHT. All data are presented as mean ± SEM. Statistical significance was determined using an unpaired two-tailed Student’s t-test. *P < 0.05; **P < 0.01; ***P < 0.05; ****P < 0.0001. Scale bars, 300 µm.

Article Snippet: Antibodies specific for human IL-1β (AF-401-NA) and mouse IL-1β (AF-201-NA) were purchased from R&D Systems (United States).

Techniques: Staining, Control, In Situ Hybridization, Two Tailed Test

Thoracotomy induces postoperative mechanical hypersensitivity progressing to CPTP. (A) Experiment designs are shown. (B and C) The changes of threshold% and mechanical pain threshold on the right chest wall at different time points after thoracotomy at the right T4 and T5 intercostal spaces. ** P < 0.01 and **** P < 0.0001 in the Thoracotomy pain or Thoracotomy no pain group vs Sham group; && P < 0.01, &&& P < 0.001, and &&&& P < 0.0001 in the Thoracotomy pain vs Thoracotomy no pain group. The data were analyzed by 2-way ANOVA followed by Tukey multiple comparisons test, n = 13 in each group. (D) Mechanical hyperalgesia ratio at different time points after thoracotomy. ANOVA, analysis of variance; CPTP, chronic post-thoracotomy pain.

Journal: Pain

Article Title: Kidney and brain-expressed protein upregulation in the anterior cingulate cortex mediates chronic post-thoracotomy pain by the phospho-protein kinase Mζ/glutamate receptor 1 signaling pathway and neuroinflammation in male rats

doi: 10.1097/j.pain.0000000000003849

Figure Lengend Snippet: Thoracotomy induces postoperative mechanical hypersensitivity progressing to CPTP. (A) Experiment designs are shown. (B and C) The changes of threshold% and mechanical pain threshold on the right chest wall at different time points after thoracotomy at the right T4 and T5 intercostal spaces. ** P < 0.01 and **** P < 0.0001 in the Thoracotomy pain or Thoracotomy no pain group vs Sham group; && P < 0.01, &&& P < 0.001, and &&&& P < 0.0001 in the Thoracotomy pain vs Thoracotomy no pain group. The data were analyzed by 2-way ANOVA followed by Tukey multiple comparisons test, n = 13 in each group. (D) Mechanical hyperalgesia ratio at different time points after thoracotomy. ANOVA, analysis of variance; CPTP, chronic post-thoracotomy pain.

Article Snippet: Then the samples were dehydrated in 30% sucrose, and cut into slices at 35 μm for immunofluorescence with antibodies against KIBRA (bs-11570R; Bioss), GluR1 (ab174785; Abcam), p -PKMζ (sc174785; Santa Cruz), TNF-α (BS-1857; Bioworld), IL-1β (AF-401-NA; R&D Systems, Minneapolis, MN), neuron-specific nuclear protein (NeuN, MAB377; Millipore, Burlington, VT), glial fibrillary acidic protein (GFAP, 3670s; Cell Signaling Technology, Danvers, MA), ionized calcium-binding adapter molecule 1 (Iba1, ab5076; Abcam), after incubation at 4°C overnight.

Techniques:

The KIBRA and p -PKMζ are activated in contralateral ACC neurons after CPTP. (A-F) Representative blots and columnar statistical charts show KIBRA, p -PKMζ, and PKMζ levels in contralateral ACC at different time points in Thoracotomy pain (A-C) or Thoracotomy no pain (D-F), * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001 vs Sham group; the data were analyzed by 1-way ANOVA followed by Tukey multiple comparisons test, n = 4∼7 rats in each group. (G-H) The photographs of the double immunofluorescence staining show that KIBRA and p -PKMζ are only colocalized with neuron markers (NeuN) but not with astrocyte marker (GFAP) and microglia marker (Iba1) in the Sham and CPTP groups. The white arrowheads indicate the co-immunostaining. Scale bar, 100 μm. ACC, anterior cingulate gyrus; ANOVA, analysis of variance; CPTP, chronic post-thoracotomy pain; GFAP, glial fibrillary acidic protein; Iba1, ionized calcium-binding adapter molecule 1; KIBRA, kidney and brain-expressed protein; NeuN, neuron-specific nuclear protein; PKMζ, protein kinase Mζ; p -PKMζ, phosphorylated protein kinase Mζ.

Journal: Pain

doi: 10.1097/j.pain.0000000000003849

Figure Lengend Snippet: The KIBRA and p -PKMζ are activated in contralateral ACC neurons after CPTP. (A-F) Representative blots and columnar statistical charts show KIBRA, p -PKMζ, and PKMζ levels in contralateral ACC at different time points in Thoracotomy pain (A-C) or Thoracotomy no pain (D-F), * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001 vs Sham group; the data were analyzed by 1-way ANOVA followed by Tukey multiple comparisons test, n = 4∼7 rats in each group. (G-H) The photographs of the double immunofluorescence staining show that KIBRA and p -PKMζ are only colocalized with neuron markers (NeuN) but not with astrocyte marker (GFAP) and microglia marker (Iba1) in the Sham and CPTP groups. The white arrowheads indicate the co-immunostaining. Scale bar, 100 μm. ACC, anterior cingulate gyrus; ANOVA, analysis of variance; CPTP, chronic post-thoracotomy pain; GFAP, glial fibrillary acidic protein; Iba1, ionized calcium-binding adapter molecule 1; KIBRA, kidney and brain-expressed protein; NeuN, neuron-specific nuclear protein; PKMζ, protein kinase Mζ; p -PKMζ, phosphorylated protein kinase Mζ.

Techniques: Double Immunofluorescence Staining, Marker, Immunostaining, Binding Assay

GluR1 and neuroinflammation in ACC neurons are involved in CPTP. (A-F) Representative blots and columnar statistical charts show GluR1, TNF-α, and IL-1β levels in contralateral ACC at different time points in Thoracotomy pain (A-C) or Thoracotomy no pain group (D-F), * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001 vs Sham group, the data were analyzed by 1-way ANOVA followed by Tukey multiple comparisons test, n = 5∼7 rats in each group. (G-I) The photographs of the double immunofluorescence staining show that GluR1, TNF-α, and IL-1β are only colocalized with neuron markers (NeuN) but not with astrocyte marker (GFAP) and microglia marker (Iba1) in the Sham and CPTP groups. The white arrowheads indicate the co-immunostaining: scale bar, 100 μm. ACC, anterior cingulate gyrus; ANOVA, analysis of variance; CPTP, chronic post-thoracotomy pain; GFAP, glial fibrillary acidic protein; GluR1, glutamate receptor 1; Iba1, ionized calcium-binding adapter molecule 1; IL-1β, interleukin-1β; NeuN, neuron-specific nuclear protein; TNF-α, tumor necrosis factor-α.

Journal: Pain

doi: 10.1097/j.pain.0000000000003849

Figure Lengend Snippet: GluR1 and neuroinflammation in ACC neurons are involved in CPTP. (A-F) Representative blots and columnar statistical charts show GluR1, TNF-α, and IL-1β levels in contralateral ACC at different time points in Thoracotomy pain (A-C) or Thoracotomy no pain group (D-F), * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001 vs Sham group, the data were analyzed by 1-way ANOVA followed by Tukey multiple comparisons test, n = 5∼7 rats in each group. (G-I) The photographs of the double immunofluorescence staining show that GluR1, TNF-α, and IL-1β are only colocalized with neuron markers (NeuN) but not with astrocyte marker (GFAP) and microglia marker (Iba1) in the Sham and CPTP groups. The white arrowheads indicate the co-immunostaining: scale bar, 100 μm. ACC, anterior cingulate gyrus; ANOVA, analysis of variance; CPTP, chronic post-thoracotomy pain; GFAP, glial fibrillary acidic protein; GluR1, glutamate receptor 1; Iba1, ionized calcium-binding adapter molecule 1; IL-1β, interleukin-1β; NeuN, neuron-specific nuclear protein; TNF-α, tumor necrosis factor-α.

Techniques: Double Immunofluorescence Staining, Marker, Immunostaining, Binding Assay

Local application of KIBRA shRNA in contralateral ACC alleviates mechanical allodynia incidents after thoracotomy. (A) Experiment designs are shown. (B) Representative blots and columnar statistical charts show KIBRA levels in contralateral ACC 28 days after rAAV-U6-shRNA (wwc1)-CMV-EGFP-pA injection, ** P < 0.01 vs Sham group. The data were analyzed by an unpaired t test. (C-F) The effect of rAAV-U6-shRNA (wwc1)-CMV-EGFP-pA (2 μL in volume) in contralateral ACC on the threshold% (C and E) and mechanical pain threshold (D-F) in rats with thoracotomy at different time points, n = 13 in Sham, Thoracotomy pain, and Thoracotomy no pain, n = 16 in KIBRA − + Thoracotomy no pain group, and n = 10 in KIBRA − + Thoracotomy pain group; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001 vs Sham group; & P < 0.05, && P < 0.01, &&& P < 0.001, and &&&& P < 0.0001 vs KIBRA − + Thoracotomy no pain or KIBRA − + Thoracotomy pain group. (G-H) Each group's area under the curve (AUC) of 0 to 21 days mechanical pain threshold were calculated. (I) Mechanical hyperalgesia ratio at different time points after KIBRA − + Thoracotomy or Thoracotomy. The data (C-F) were analyzed by 2-way ANOVA followed by Tukey multiple comparisons test, the data (G and H) were analyzed by 1-way ANOVA followed by Tukey multiple comparisons test, and the data (I) were analyzed by Fisher exact test. ACC, anterior cingulate gyrus; ANOVA, analysis of variance; KIBRA, kidney and brain-expressed protein; shRNA, short hairpin RNA.

Journal: Pain

doi: 10.1097/j.pain.0000000000003849

Figure Lengend Snippet: Local application of KIBRA shRNA in contralateral ACC alleviates mechanical allodynia incidents after thoracotomy. (A) Experiment designs are shown. (B) Representative blots and columnar statistical charts show KIBRA levels in contralateral ACC 28 days after rAAV-U6-shRNA (wwc1)-CMV-EGFP-pA injection, ** P < 0.01 vs Sham group. The data were analyzed by an unpaired t test. (C-F) The effect of rAAV-U6-shRNA (wwc1)-CMV-EGFP-pA (2 μL in volume) in contralateral ACC on the threshold% (C and E) and mechanical pain threshold (D-F) in rats with thoracotomy at different time points, n = 13 in Sham, Thoracotomy pain, and Thoracotomy no pain, n = 16 in KIBRA − + Thoracotomy no pain group, and n = 10 in KIBRA − + Thoracotomy pain group; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001 vs Sham group; & P < 0.05, && P < 0.01, &&& P < 0.001, and &&&& P < 0.0001 vs KIBRA − + Thoracotomy no pain or KIBRA − + Thoracotomy pain group. (G-H) Each group's area under the curve (AUC) of 0 to 21 days mechanical pain threshold were calculated. (I) Mechanical hyperalgesia ratio at different time points after KIBRA − + Thoracotomy or Thoracotomy. The data (C-F) were analyzed by 2-way ANOVA followed by Tukey multiple comparisons test, the data (G and H) were analyzed by 1-way ANOVA followed by Tukey multiple comparisons test, and the data (I) were analyzed by Fisher exact test. ACC, anterior cingulate gyrus; ANOVA, analysis of variance; KIBRA, kidney and brain-expressed protein; shRNA, short hairpin RNA.

Techniques: shRNA, Injection

Knockdown of KIBRA in contralateral ACC prevents the upregulation of KIBRA, p -PKMζ/GluR1 signaling pathways, and neuroinflammation in CPTP rats. (A-F) Representative blots and columnar statistical charts show KIBRA, p -PKMζ, PKMζ, TNF-α, and IL-1β levels in ACC analyzed 21 days after the sham operation, thoracotomy, or KIBRA − + thoracotomy. The data were analyzed by 1-way ANOVA followed by Tukey multiple comparisons test, n = 4∼8 rats in each group. ACC, anterior cingulate gyrus; CPTP, chronic post-thoracotomy pain; GluR1, glutamate receptor 1; IL-1β, interleukin-1β; KIBRA, kidney and brain-expressed protein; PKMζ, protein kinase Mζ; p -PKMζ, phosphorylated protein kinase Mζ; TNF-α, tumor necrosis factor-α.

Journal: Pain

doi: 10.1097/j.pain.0000000000003849

Figure Lengend Snippet: Knockdown of KIBRA in contralateral ACC prevents the upregulation of KIBRA, p -PKMζ/GluR1 signaling pathways, and neuroinflammation in CPTP rats. (A-F) Representative blots and columnar statistical charts show KIBRA, p -PKMζ, PKMζ, TNF-α, and IL-1β levels in ACC analyzed 21 days after the sham operation, thoracotomy, or KIBRA − + thoracotomy. The data were analyzed by 1-way ANOVA followed by Tukey multiple comparisons test, n = 4∼8 rats in each group. ACC, anterior cingulate gyrus; CPTP, chronic post-thoracotomy pain; GluR1, glutamate receptor 1; IL-1β, interleukin-1β; KIBRA, kidney and brain-expressed protein; PKMζ, protein kinase Mζ; p -PKMζ, phosphorylated protein kinase Mζ; TNF-α, tumor necrosis factor-α.

Techniques: Knockdown, Protein-Protein interactions

Overexpression of KIBRA in ACC causes allodynia and activates p -PKMζ/GluR1 signaling pathways and neuroinflammation. (A) Experiment designs are shown. (B) Mechanical hyperalgesia ratio on 7, 14, and 21 days after thoracotomy or KIBRA overexpression. **** P < 0.0001 vs Thoracotomy pain group; the data were analyzed by Fisher exact test. (C and D) The threshold% and mechanical pain threshold at different time points for pain rats after injection of rAAV-CMV-wwc1-3xFLAG-WPREs or thoracotomy, * P < 0.05, *** P < 0.001, and **** P < 0.0001 vs Sham group, &&&& P < 0.00001 vs KIBRA + pain group, the data were analyzed by 2-way ANOVA followed by Tukey multiple comparisons test, n = 8 in Sham, n = 13 in Thoracotomy pain, n = 12 in KIBRA + pain, n = 8 in KIBRA + no pain group. (E-J) Representative blots and columnar statistical charts show KIBRA, p -PKMζ, PKMζ, GluR1, TNF-α, and IL-1β levels in ACC analyzed 21 days in Sham, KIBRA + pain, and KIBRA + no pain rats. The data were analyzed by 1-way ANOVA followed by Tukey multiple comparisons test, n = 4 in each group. ACC, anterior cingulate gyrus; ANOVA, analysis of variance; GluR1, glutamate receptor 1; IL-1β, interleukin-1β; KIBRA, kidney and brain-expressed protein; PKMζ, protein kinase Mζ; p -PKMζ, phosphorylated protein kinase Mζ; TNF-α, tumor necrosis factor-α.

Journal: Pain

doi: 10.1097/j.pain.0000000000003849

Figure Lengend Snippet: Overexpression of KIBRA in ACC causes allodynia and activates p -PKMζ/GluR1 signaling pathways and neuroinflammation. (A) Experiment designs are shown. (B) Mechanical hyperalgesia ratio on 7, 14, and 21 days after thoracotomy or KIBRA overexpression. **** P < 0.0001 vs Thoracotomy pain group; the data were analyzed by Fisher exact test. (C and D) The threshold% and mechanical pain threshold at different time points for pain rats after injection of rAAV-CMV-wwc1-3xFLAG-WPREs or thoracotomy, * P < 0.05, *** P < 0.001, and **** P < 0.0001 vs Sham group, &&&& P < 0.00001 vs KIBRA + pain group, the data were analyzed by 2-way ANOVA followed by Tukey multiple comparisons test, n = 8 in Sham, n = 13 in Thoracotomy pain, n = 12 in KIBRA + pain, n = 8 in KIBRA + no pain group. (E-J) Representative blots and columnar statistical charts show KIBRA, p -PKMζ, PKMζ, GluR1, TNF-α, and IL-1β levels in ACC analyzed 21 days in Sham, KIBRA + pain, and KIBRA + no pain rats. The data were analyzed by 1-way ANOVA followed by Tukey multiple comparisons test, n = 4 in each group. ACC, anterior cingulate gyrus; ANOVA, analysis of variance; GluR1, glutamate receptor 1; IL-1β, interleukin-1β; KIBRA, kidney and brain-expressed protein; PKMζ, protein kinase Mζ; p -PKMζ, phosphorylated protein kinase Mζ; TNF-α, tumor necrosis factor-α.

Techniques: Over Expression, Protein-Protein interactions, Injection

ACC overexpression KIBRA combined with thoracotomy induced CPTP in all rats. (A) Experiment designs are shown. (B) Incidence of pain on 7, 14, and 21 days after thoracotomy in KIBRA overexpression rats. ** P < 0.01 vs Thoracotomy pain group; the data were analyzed by Fisher exact test. (C and D) The threshold% and mechanical pain threshold at different time points in KIBRA + no pain + Thoracotomy pain, Thoracotomy pain, or Sham group, **** P < 0.0001 vs Sham group, & P < 0.05 vs Thoracotomy pain group. The data were analyzed by 2-way ANOVA followed by Tukey multiple comparisons test, n = 8 in Sham, n = 13 in Thoracotomy pain, n = 14 in KIBRA + no pain + Thoracotomy pain group. (E-J) Representative blots and columnar statistical charts show KIBRA, p -PKMζ, PKMζ, GluR1, TNF-α, and IL-1β levels in ACC analyzed on POD21 in Sham, Thoracotomy pain, or KIBRA + no pain + Thoracotomy pain rats, n = 4 rats in each group. The data were analyzed by 1-way ANOVA followed by Tukey post hoc test. ACC, anterior cingulate gyrus; ANOVA, analysis of variance; CPTP, chronic post-thoracotomy pain; GluR1, glutamate receptor 1; IL-1β, interleukin-1β; KIBRA, kidney and brain-expressed protein; PKMζ, protein kinase Mζ; p -PKMζ, phosphorylated protein kinase Mζ; TNF-α, tumor necrosis factor-α.

Journal: Pain

doi: 10.1097/j.pain.0000000000003849

Figure Lengend Snippet: ACC overexpression KIBRA combined with thoracotomy induced CPTP in all rats. (A) Experiment designs are shown. (B) Incidence of pain on 7, 14, and 21 days after thoracotomy in KIBRA overexpression rats. ** P < 0.01 vs Thoracotomy pain group; the data were analyzed by Fisher exact test. (C and D) The threshold% and mechanical pain threshold at different time points in KIBRA + no pain + Thoracotomy pain, Thoracotomy pain, or Sham group, **** P < 0.0001 vs Sham group, & P < 0.05 vs Thoracotomy pain group. The data were analyzed by 2-way ANOVA followed by Tukey multiple comparisons test, n = 8 in Sham, n = 13 in Thoracotomy pain, n = 14 in KIBRA + no pain + Thoracotomy pain group. (E-J) Representative blots and columnar statistical charts show KIBRA, p -PKMζ, PKMζ, GluR1, TNF-α, and IL-1β levels in ACC analyzed on POD21 in Sham, Thoracotomy pain, or KIBRA + no pain + Thoracotomy pain rats, n = 4 rats in each group. The data were analyzed by 1-way ANOVA followed by Tukey post hoc test. ACC, anterior cingulate gyrus; ANOVA, analysis of variance; CPTP, chronic post-thoracotomy pain; GluR1, glutamate receptor 1; IL-1β, interleukin-1β; KIBRA, kidney and brain-expressed protein; PKMζ, protein kinase Mζ; p -PKMζ, phosphorylated protein kinase Mζ; TNF-α, tumor necrosis factor-α.

Techniques: Over Expression

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