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il 1β wl00891  (Proteintech)


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    Proteintech il 1β wl00891
    CSP NPs inhibit NF-κB/NLRP3 signaling pathway during vascular calcification. Rat vascular smooth muscle cells (VSMCs) were treated with growth medium (GM), calcifying medium (CM), or CM with CSP NPs (2, 5, and 10 μg/mL) for 7 days (n = 4). (A) Representative western blots of p-p65 and p65. (B) Quantification of p-p65 protein expression by densitometry. Rat VSMCs were treated with GM, CM, or CM with CSP NPs (10 μg/mL) for 7 days (n = 4). (C) Representative immunostaining images of p65. Nuclear localization of p65 was determined by confocal microscopy. Scale bar = 25 μm. Rat VSMCs were treated with GM, CM, or CM with CSP NPs (2, 5, and 10 μg/mL) for 7 days (n = 4). (D) Representative western blots of NLRP3, <t>Cleaved-Caspase1,</t> <t>IL-1β,</t> and IL-6. (E) Quantification of NLRP3, Cleaved-Caspase1, IL-1β, and IL-6 protein expression by densitometry. VitD 3 -overloaded mice were treated with CSP NPs (1 mg/kg) for 8 days (n = 6). (F) Representative western blots of p-p65, p65, and NLRP3. (G) Quantification of p-p65 and NLRP3 protein expression by densitometry. Rats subjected to 5/6 nephrectomy were treated with CSP NPs (0.7 mg/kg) for 4 weeks (n = 6). (H) Representative western blots of p-p65, p65, and NLRP3. (I) Quantification of p-p65 and NLRP3 protein expression by densitometry. ∗ P< 0.05, ∗∗ P< 0.01.
    Il 1β Wl00891, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 2005 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Ultrasmall Cu 2−x Se nanoparticles alleviate vascular calcification through inhibiting oxidative stress and NF-κB/NLRP3-mediated inflammation"

    Article Title: Ultrasmall Cu 2−x Se nanoparticles alleviate vascular calcification through inhibiting oxidative stress and NF-κB/NLRP3-mediated inflammation

    Journal: Redox Biology

    doi: 10.1016/j.redox.2025.103961

    CSP NPs inhibit NF-κB/NLRP3 signaling pathway during vascular calcification. Rat vascular smooth muscle cells (VSMCs) were treated with growth medium (GM), calcifying medium (CM), or CM with CSP NPs (2, 5, and 10 μg/mL) for 7 days (n = 4). (A) Representative western blots of p-p65 and p65. (B) Quantification of p-p65 protein expression by densitometry. Rat VSMCs were treated with GM, CM, or CM with CSP NPs (10 μg/mL) for 7 days (n = 4). (C) Representative immunostaining images of p65. Nuclear localization of p65 was determined by confocal microscopy. Scale bar = 25 μm. Rat VSMCs were treated with GM, CM, or CM with CSP NPs (2, 5, and 10 μg/mL) for 7 days (n = 4). (D) Representative western blots of NLRP3, Cleaved-Caspase1, IL-1β, and IL-6. (E) Quantification of NLRP3, Cleaved-Caspase1, IL-1β, and IL-6 protein expression by densitometry. VitD 3 -overloaded mice were treated with CSP NPs (1 mg/kg) for 8 days (n = 6). (F) Representative western blots of p-p65, p65, and NLRP3. (G) Quantification of p-p65 and NLRP3 protein expression by densitometry. Rats subjected to 5/6 nephrectomy were treated with CSP NPs (0.7 mg/kg) for 4 weeks (n = 6). (H) Representative western blots of p-p65, p65, and NLRP3. (I) Quantification of p-p65 and NLRP3 protein expression by densitometry. ∗ P< 0.05, ∗∗ P< 0.01.
    Figure Legend Snippet: CSP NPs inhibit NF-κB/NLRP3 signaling pathway during vascular calcification. Rat vascular smooth muscle cells (VSMCs) were treated with growth medium (GM), calcifying medium (CM), or CM with CSP NPs (2, 5, and 10 μg/mL) for 7 days (n = 4). (A) Representative western blots of p-p65 and p65. (B) Quantification of p-p65 protein expression by densitometry. Rat VSMCs were treated with GM, CM, or CM with CSP NPs (10 μg/mL) for 7 days (n = 4). (C) Representative immunostaining images of p65. Nuclear localization of p65 was determined by confocal microscopy. Scale bar = 25 μm. Rat VSMCs were treated with GM, CM, or CM with CSP NPs (2, 5, and 10 μg/mL) for 7 days (n = 4). (D) Representative western blots of NLRP3, Cleaved-Caspase1, IL-1β, and IL-6. (E) Quantification of NLRP3, Cleaved-Caspase1, IL-1β, and IL-6 protein expression by densitometry. VitD 3 -overloaded mice were treated with CSP NPs (1 mg/kg) for 8 days (n = 6). (F) Representative western blots of p-p65, p65, and NLRP3. (G) Quantification of p-p65 and NLRP3 protein expression by densitometry. Rats subjected to 5/6 nephrectomy were treated with CSP NPs (0.7 mg/kg) for 4 weeks (n = 6). (H) Representative western blots of p-p65, p65, and NLRP3. (I) Quantification of p-p65 and NLRP3 protein expression by densitometry. ∗ P< 0.05, ∗∗ P< 0.01.

    Techniques Used: Western Blot, Expressing, Immunostaining, Confocal Microscopy



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    CSP NPs inhibit NF-κB/NLRP3 signaling pathway during vascular calcification. Rat vascular smooth muscle cells (VSMCs) were treated with growth medium (GM), calcifying medium (CM), or CM with CSP NPs (2, 5, and 10 μg/mL) for 7 days (n = 4). (A) Representative western blots of p-p65 and p65. (B) Quantification of p-p65 protein expression by densitometry. Rat VSMCs were treated with GM, CM, or CM with CSP NPs (10 μg/mL) for 7 days (n = 4). (C) Representative immunostaining images of p65. Nuclear localization of p65 was determined by confocal microscopy. Scale bar = 25 μm. Rat VSMCs were treated with GM, CM, or CM with CSP NPs (2, 5, and 10 μg/mL) for 7 days (n = 4). (D) Representative western blots of NLRP3, <t>Cleaved-Caspase1,</t> <t>IL-1β,</t> and IL-6. (E) Quantification of NLRP3, Cleaved-Caspase1, IL-1β, and IL-6 protein expression by densitometry. VitD 3 -overloaded mice were treated with CSP NPs (1 mg/kg) for 8 days (n = 6). (F) Representative western blots of p-p65, p65, and NLRP3. (G) Quantification of p-p65 and NLRP3 protein expression by densitometry. Rats subjected to 5/6 nephrectomy were treated with CSP NPs (0.7 mg/kg) for 4 weeks (n = 6). (H) Representative western blots of p-p65, p65, and NLRP3. (I) Quantification of p-p65 and NLRP3 protein expression by densitometry. ∗ P< 0.05, ∗∗ P< 0.01.
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    Primary Antibodies Used in the Study
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    Image Search Results


    CSP NPs inhibit NF-κB/NLRP3 signaling pathway during vascular calcification. Rat vascular smooth muscle cells (VSMCs) were treated with growth medium (GM), calcifying medium (CM), or CM with CSP NPs (2, 5, and 10 μg/mL) for 7 days (n = 4). (A) Representative western blots of p-p65 and p65. (B) Quantification of p-p65 protein expression by densitometry. Rat VSMCs were treated with GM, CM, or CM with CSP NPs (10 μg/mL) for 7 days (n = 4). (C) Representative immunostaining images of p65. Nuclear localization of p65 was determined by confocal microscopy. Scale bar = 25 μm. Rat VSMCs were treated with GM, CM, or CM with CSP NPs (2, 5, and 10 μg/mL) for 7 days (n = 4). (D) Representative western blots of NLRP3, Cleaved-Caspase1, IL-1β, and IL-6. (E) Quantification of NLRP3, Cleaved-Caspase1, IL-1β, and IL-6 protein expression by densitometry. VitD 3 -overloaded mice were treated with CSP NPs (1 mg/kg) for 8 days (n = 6). (F) Representative western blots of p-p65, p65, and NLRP3. (G) Quantification of p-p65 and NLRP3 protein expression by densitometry. Rats subjected to 5/6 nephrectomy were treated with CSP NPs (0.7 mg/kg) for 4 weeks (n = 6). (H) Representative western blots of p-p65, p65, and NLRP3. (I) Quantification of p-p65 and NLRP3 protein expression by densitometry. ∗ P< 0.05, ∗∗ P< 0.01.

    Journal: Redox Biology

    Article Title: Ultrasmall Cu 2−x Se nanoparticles alleviate vascular calcification through inhibiting oxidative stress and NF-κB/NLRP3-mediated inflammation

    doi: 10.1016/j.redox.2025.103961

    Figure Lengend Snippet: CSP NPs inhibit NF-κB/NLRP3 signaling pathway during vascular calcification. Rat vascular smooth muscle cells (VSMCs) were treated with growth medium (GM), calcifying medium (CM), or CM with CSP NPs (2, 5, and 10 μg/mL) for 7 days (n = 4). (A) Representative western blots of p-p65 and p65. (B) Quantification of p-p65 protein expression by densitometry. Rat VSMCs were treated with GM, CM, or CM with CSP NPs (10 μg/mL) for 7 days (n = 4). (C) Representative immunostaining images of p65. Nuclear localization of p65 was determined by confocal microscopy. Scale bar = 25 μm. Rat VSMCs were treated with GM, CM, or CM with CSP NPs (2, 5, and 10 μg/mL) for 7 days (n = 4). (D) Representative western blots of NLRP3, Cleaved-Caspase1, IL-1β, and IL-6. (E) Quantification of NLRP3, Cleaved-Caspase1, IL-1β, and IL-6 protein expression by densitometry. VitD 3 -overloaded mice were treated with CSP NPs (1 mg/kg) for 8 days (n = 6). (F) Representative western blots of p-p65, p65, and NLRP3. (G) Quantification of p-p65 and NLRP3 protein expression by densitometry. Rats subjected to 5/6 nephrectomy were treated with CSP NPs (0.7 mg/kg) for 4 weeks (n = 6). (H) Representative western blots of p-p65, p65, and NLRP3. (I) Quantification of p-p65 and NLRP3 protein expression by densitometry. ∗ P< 0.05, ∗∗ P< 0.01.

    Article Snippet: IL-1β (WL00891) and IL-6 (WL02841) primary antibodies were purchased from Wanleibio (China). β-actin (HRP-66009) primary antibody was purchased from Proteintech (USA).

    Techniques: Western Blot, Expressing, Immunostaining, Confocal Microscopy

    Primary Antibodies Used in the Study

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: CD38 Deficiency Protects Mouse Retinal Ganglion Cells Through Activating the NAD+/Sirt1 Pathway in Ischemia-Reperfusion and Optic Nerve Crush Models

    doi: 10.1167/iovs.65.5.36

    Figure Lengend Snippet: Primary Antibodies Used in the Study

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    Techniques:

    Expression and localization of CD38 in WT rat and mouse retinal tissues. ( A ) Detection of CD38 protein expression in mouse heart, rat retina, and mouse retina by WB. ( B ) Quantitative analysis of CD38 protein expression. ( C ) Quantitative analysis of CD38 mRNA expression in mouse retina. ( D ) Quantification of CD38 mRNA expression in rat retina. ( E ) Localization of CD38 in mouse liver by immunofluorescence. ( F ) Localization of CD38 in rat retina by immunofluorescence. ( G ) Localization of CD38 in mouse retina detected by immunofluorescence. ( H ) Cellular localization of CD38 in the mouse retina determined by GS and CD38 immunofluorescence double staining. GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; OPL, outer plexiform layer; ONL, outer nuclear layer; WT, wild type; GS, marker for Müller cells; data presented as: mean ± SEM; ns, not significant; * P < 0.05; *** P < 0.001.

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: CD38 Deficiency Protects Mouse Retinal Ganglion Cells Through Activating the NAD+/Sirt1 Pathway in Ischemia-Reperfusion and Optic Nerve Crush Models

    doi: 10.1167/iovs.65.5.36

    Figure Lengend Snippet: Expression and localization of CD38 in WT rat and mouse retinal tissues. ( A ) Detection of CD38 protein expression in mouse heart, rat retina, and mouse retina by WB. ( B ) Quantitative analysis of CD38 protein expression. ( C ) Quantitative analysis of CD38 mRNA expression in mouse retina. ( D ) Quantification of CD38 mRNA expression in rat retina. ( E ) Localization of CD38 in mouse liver by immunofluorescence. ( F ) Localization of CD38 in rat retina by immunofluorescence. ( G ) Localization of CD38 in mouse retina detected by immunofluorescence. ( H ) Cellular localization of CD38 in the mouse retina determined by GS and CD38 immunofluorescence double staining. GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; OPL, outer plexiform layer; ONL, outer nuclear layer; WT, wild type; GS, marker for Müller cells; data presented as: mean ± SEM; ns, not significant; * P < 0.05; *** P < 0.001.

    Article Snippet: IL-1β , Wanleibio , WL00891 , Rabbit polyclonal , 1:1000 (WB).

    Techniques: Expressing, Immunofluorescence, Double Staining, Marker

    Effect of CD38 KO on retinal glial activation in mice in the I/R model. ( A ) GFAP immunofluorescence staining of paraffin sections of mouse retinas. ( B ) Quantitative statistics of GFAP immunofluorescence staining of paraffin sections of mouse retina. ( C ) The expression of CD38 protein in retina was detected by WB in sham operation group and I/R on day 1, day 3, and day 7. ( D ) The expression of GFAP proteins in retina was detected by WB in the sham operation group and I/R on day 1, day 3, and day 7. ( E ) WB was used to detect changes in CD38 protein expression in retinas at 3 days of I/R in WT and KO mice. GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; OPL, outer plexiform layer; ONL, outer nuclear layer. Scale bars = 50 µm; WT, wild type; KO, knockout; data presented as mean ± SEM. * P < 0.05, ** P < 0.01.

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: CD38 Deficiency Protects Mouse Retinal Ganglion Cells Through Activating the NAD+/Sirt1 Pathway in Ischemia-Reperfusion and Optic Nerve Crush Models

    doi: 10.1167/iovs.65.5.36

    Figure Lengend Snippet: Effect of CD38 KO on retinal glial activation in mice in the I/R model. ( A ) GFAP immunofluorescence staining of paraffin sections of mouse retinas. ( B ) Quantitative statistics of GFAP immunofluorescence staining of paraffin sections of mouse retina. ( C ) The expression of CD38 protein in retina was detected by WB in sham operation group and I/R on day 1, day 3, and day 7. ( D ) The expression of GFAP proteins in retina was detected by WB in the sham operation group and I/R on day 1, day 3, and day 7. ( E ) WB was used to detect changes in CD38 protein expression in retinas at 3 days of I/R in WT and KO mice. GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; OPL, outer plexiform layer; ONL, outer nuclear layer. Scale bars = 50 µm; WT, wild type; KO, knockout; data presented as mean ± SEM. * P < 0.05, ** P < 0.01.

    Article Snippet: IL-1β , Wanleibio , WL00891 , Rabbit polyclonal , 1:1000 (WB).

    Techniques: Activation Assay, Immunofluorescence, Staining, Expressing, Knock-Out

    Changes in Sirt1 and CD38 protein expression and assessment of the degree of deacetylation of downstream molecules in the ONC model. ( A ) The expression of Sirt1 protein in retina was detected by WB in the sham operation group and crush on day 3, day 7, and day 14. ( B ) The expression of CD38 protein in retina was detected by WB in the sham operation group and crush on day 3, day 7, and day 14. ( C ) The expression of Ac-p53 protein in retina was detected by WB in the sham operation group and crush on day 3, day 7, and day 14. ( D ) The expression of Ac-p65 protein in retina was detected by WB in the sham operation group and crush on day 3, day 7, and day 14. ( E ) The expression of IL-1β protein in retina was detected by WB in the sham operation group and crush on day 3, day 7, and day 14. ( F ) The expression of Caspase3 protein in retina was detected by WB in the sham operation group and crush on day 3, day 7, and day 14. WT, wild type; KO, knockout; data presented as: mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: CD38 Deficiency Protects Mouse Retinal Ganglion Cells Through Activating the NAD+/Sirt1 Pathway in Ischemia-Reperfusion and Optic Nerve Crush Models

    doi: 10.1167/iovs.65.5.36

    Figure Lengend Snippet: Changes in Sirt1 and CD38 protein expression and assessment of the degree of deacetylation of downstream molecules in the ONC model. ( A ) The expression of Sirt1 protein in retina was detected by WB in the sham operation group and crush on day 3, day 7, and day 14. ( B ) The expression of CD38 protein in retina was detected by WB in the sham operation group and crush on day 3, day 7, and day 14. ( C ) The expression of Ac-p53 protein in retina was detected by WB in the sham operation group and crush on day 3, day 7, and day 14. ( D ) The expression of Ac-p65 protein in retina was detected by WB in the sham operation group and crush on day 3, day 7, and day 14. ( E ) The expression of IL-1β protein in retina was detected by WB in the sham operation group and crush on day 3, day 7, and day 14. ( F ) The expression of Caspase3 protein in retina was detected by WB in the sham operation group and crush on day 3, day 7, and day 14. WT, wild type; KO, knockout; data presented as: mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: IL-1β , Wanleibio , WL00891 , Rabbit polyclonal , 1:1000 (WB).

    Techniques: Expressing, Knock-Out

    To evaluate the effect of CD38 deletion on NAD+ content, acetylated protein content, and inflammatory and apoptotic protein expression in the retina in the optic nerve crush model. ( A ) In the crush day 7 model, the NAD+ kit was used to detect the changes of NAD + content in the retina of WT and KO mice. ( B ) In the crush day 7 model, the expression of Sirt1 protein in the retina of WT and KO mice was detected by WB. ( C ) In the crush day 7 model, the expression of Ac-p65 protein in the retina of WT and KO mice was detected by WB. ( D ) In the crush day 7 model, the expression of Ac-p53 protein in WT and KO retinas was detected by WB. (E) In the crush day 7 model, the expression of TNF-α protein in the retina of WT and KO mice was detected by WB. ( F ) In the crush day 7 model, WB was used to detect the changes of IL-1β protein expression in the retina of WT and KO mice. ( G ) In the crush day 3 model, WB was used to detect changes in Caspase3 protein expression in the retina of WT and KO mice. WT, wild type; KO, knockout; data presented as: mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: CD38 Deficiency Protects Mouse Retinal Ganglion Cells Through Activating the NAD+/Sirt1 Pathway in Ischemia-Reperfusion and Optic Nerve Crush Models

    doi: 10.1167/iovs.65.5.36

    Figure Lengend Snippet: To evaluate the effect of CD38 deletion on NAD+ content, acetylated protein content, and inflammatory and apoptotic protein expression in the retina in the optic nerve crush model. ( A ) In the crush day 7 model, the NAD+ kit was used to detect the changes of NAD + content in the retina of WT and KO mice. ( B ) In the crush day 7 model, the expression of Sirt1 protein in the retina of WT and KO mice was detected by WB. ( C ) In the crush day 7 model, the expression of Ac-p65 protein in the retina of WT and KO mice was detected by WB. ( D ) In the crush day 7 model, the expression of Ac-p53 protein in WT and KO retinas was detected by WB. (E) In the crush day 7 model, the expression of TNF-α protein in the retina of WT and KO mice was detected by WB. ( F ) In the crush day 7 model, WB was used to detect the changes of IL-1β protein expression in the retina of WT and KO mice. ( G ) In the crush day 3 model, WB was used to detect changes in Caspase3 protein expression in the retina of WT and KO mice. WT, wild type; KO, knockout; data presented as: mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: IL-1β , Wanleibio , WL00891 , Rabbit polyclonal , 1:1000 (WB).

    Techniques: Expressing, Knock-Out