human il 1β  (Proteintech)

Journal: Materials Today Bio

Article Title: Ultrasound-responsive CPS piezoelectric hydrogel synergistically repairs annulus fibrosus defects through immune reprogramming and cell recruitment

doi: 10.1016/j.mtbio.2026.102825

Figure Lengend Snippet: Assessment of the anti-inflammatory capacity of CPS gel in vitro . A Schematic of the co-culture of hydrogel with RAW 264.7. B Quantification of the relative fluorescence intensity of TNF-α. C Quantification of the relative fluorescence intensity of IL-1β. D Immunofluorescence image of TNF-α expression in RAW 264.7 (Scale bar = 50 μm). E Immunofluorescence image of IL-1β expression in RAW 264.7 (Scale bar = 50 μm). F-H The protein expression level of TNF-α and IL-1β was evaluated by WB and quantified by ImageJ. Data are mean ± SD (n = 3). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Staining was performed using IL-1β (Bioss, BS-0812R) and TNF-α (Santa, SC-52746) probes, and the staining was observed under a fluorescent inverted microscope.

Techniques: In Vitro, Co-Culture Assay, Fluorescence, Immunofluorescence, Expressing

Journal: Materials Today Bio

Article Title: Ultrasound-responsive CPS piezoelectric hydrogel synergistically repairs annulus fibrosus defects through immune reprogramming and cell recruitment

doi: 10.1016/j.mtbio.2026.102825

Figure Lengend Snippet: In vivo study of CPS gel for AF repair. A H&E, S&O staining sections of rat IVD at 4W and 8W post-operation (scale bar = 1 mm). B Col-1, IL-1β IHC staining sections of rat IVD at 4W and 8W post-operation (Scale bar = 50 μm). C Postoperative 4W Col-1 quantitative analysis. D Postoperative 8W Col-1 quantitative analysis. E. Postoperative 4W IL-1β quantitative analysis. F Postoperative 8W IL-1β quantitative analysis. Data are mean ± SD (n = 3). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Staining was performed using IL-1β (Bioss, BS-0812R) and TNF-α (Santa, SC-52746) probes, and the staining was observed under a fluorescent inverted microscope.

Techniques: In Vivo, Staining, Immunohistochemistry

Journal: JBMR Plus

Article Title: USP34 attenuates cartilage degradation in temporomandibular joint osteoarthritis by ANT1-mediated mitophagy

doi: 10.1093/jbmrpl/ziag004

Figure Lengend Snippet: Deletion of Usp34 accelerates cartilage destruction during TMJ OA. (A) Representative images of Safranin O/Fast Green staining of SHAM and UBR-induced TMJ OA mice. Scale bars: 100 μm for low and 50 μm for high magnification. (B and C) Quantitative analysis regarding cartilage thickness and modified Mankin score according to Safranin O/Fast Green staining. n = 6 per group. (D) Representative micro-CT images reveal the subchondral bone microstructure. Scale bars: 100 μm. (E) Quantitative analysis of subchondral bone parameters. (F and G) Representative images and quantitative analysis of western blot for MMP13, ADAMTS5, α-tubulin in ATDC5 cells transfected with Usp34 siRNA following exposure to IL-1β. (H) Relative mRNA expression of MMP3, MMP13, ADAMTS4, and ADAMTS5 in ATDC5 cells transfected with Usp34 siRNA following exposure to IL-1β.

Article Snippet: To model the inflammatory microenvironment of TMJ OA, ATDC5 cells (1 × 10 5 /well) were cultured in 24-well plates, followed by treatment with 10 ng/mL IL-1β (HY-P7073A; MedChemExpress).

Techniques: Staining, Modification, Micro-CT, Western Blot, Transfection, Expressing

Journal: JBMR Plus

Article Title: USP34 attenuates cartilage degradation in temporomandibular joint osteoarthritis by ANT1-mediated mitophagy

doi: 10.1093/jbmrpl/ziag004

Figure Lengend Snippet: USP34 deubiquitinates and stabilizes ANT1. (A) Volcano plots showing the differentially expressed proteins of USP34-deficient cells from public proteomic dataset in the National Genomics Data Center under accession numbers: OMIX007639. (B) Heatmap showing the differentially expressed protein of USP34-deficient cells from public proteomic dataset (OMIX007639). (C and D) Representative images and quantitative analysis of western blot for ANT1 and α-tubulin in ATDC5 cells transfected with Usp34 siRNA following exposure to IL-1β. (E) Representative images of immunofluorescence staining of ANT1 in the TMJ cartilages of SHAM and UBR-induced TMJ OA mice. Scale bars: 50 μm. (F) Co-immunoprecipitation of USP34 with ectopically expressed ANT1 in HEK293T cells. (G) Immunoblot of ANT1-linked polyubiquitin. HEK293T cells were treated with 10 μM MG132 for 4 h after transfection with the indicated constructs. The cell lysates were subjected to immunoprecipitation with the indicated antibody. (H) Measurement of ANT1 degradation rate. HEK293T cells were transfected with the indicated constructs and treated with 10 mg/mL CHX.

Article Snippet: To model the inflammatory microenvironment of TMJ OA, ATDC5 cells (1 × 10 5 /well) were cultured in 24-well plates, followed by treatment with 10 ng/mL IL-1β (HY-P7073A; MedChemExpress).

Techniques: Western Blot, Transfection, Immunofluorescence, Staining, Immunoprecipitation, Construct

Journal: JBMR Plus

Article Title: USP34 attenuates cartilage degradation in temporomandibular joint osteoarthritis by ANT1-mediated mitophagy

doi: 10.1093/jbmrpl/ziag004

Figure Lengend Snippet: ANT1 overexpression rescues mitochondrial homeostasis in USP34-deficient cells. (A and B) Representative images and quantitative analysis of western blot for LC3, Parkin, PINK1, and α-tubulin in ATDC5 cells transfected with Usp34 siRNA or Lv-ANT1 , following exposure to IL-1β. (C) Representative TEM images of ATDC5 cells transfected with Usp34 siRNA or Lv-ANT1 . Subcellular structures with discernible mitochondria (yellow arrows) and bound by a double limiting membrane are identified as putative mitophagosome structures (red arrows). Scale bars: 200 nm. (D) ATDC5 cells stained with mitotracker and lysotracker after transfection with Usp34 siRNA or Lv-ANT1 . Scale bars: 20 μm. (E) ATDC5 cells stained with Mito-SOX after transfection with Usp34 siRNA or Lv-ANT1 . Scale bars: 20 μm.

Article Snippet: To model the inflammatory microenvironment of TMJ OA, ATDC5 cells (1 × 10 5 /well) were cultured in 24-well plates, followed by treatment with 10 ng/mL IL-1β (HY-P7073A; MedChemExpress).

Techniques: Over Expression, Western Blot, Transfection, Membrane, Staining

Journal: JBMR Plus

Article Title: USP34 attenuates cartilage degradation in temporomandibular joint osteoarthritis by ANT1-mediated mitophagy

doi: 10.1093/jbmrpl/ziag004

Figure Lengend Snippet: USP34 overexpression enhanced chondrocyte viability. (A and B) Representative images and quantitative analysis of western blot for LC3, Parkin, PINK1, and α-tubulin in ATDC5 cells transfected with Usp34 lentiviral activation particles ( Usp34 ac) following exposure to IL-1β. (C and D) Representative images and quantitative analysis of western blot for MMP13, ADAMTS5, and α-tubulin in ATDC5 cells transfected with Usp34 ac following exposure to IL-1β. (E and F) Representative images and quantitative analysis of western blot for MMP13, ADAMTS5, and α-tubulin in ATDC5 cells with the indicated treatment. (G) ATDC5 cells stained with Acan and Col2a1 after transfection with Usp34 ac or Lv-ANT1 . Scale bars: 50 μm. (H and I) Relative mRNA expression of Acan and Col2a1 in ATDC5 cells with the indicated treatments.

Article Snippet: To model the inflammatory microenvironment of TMJ OA, ATDC5 cells (1 × 10 5 /well) were cultured in 24-well plates, followed by treatment with 10 ng/mL IL-1β (HY-P7073A; MedChemExpress).

Techniques: Over Expression, Western Blot, Transfection, Activation Assay, Staining, Expressing

Journal: Biochemistry and Biophysics Reports

Article Title: LncRNA RMST knockout inhibits fibrosis by down-regulating Smad3 during mouse skin wound healing

doi: 10.1016/j.bbrep.2025.102386

Figure Lengend Snippet: RMST-KO reduces fibrosis in mouse skin wound healing. (A) Differences of RMST expression between unwounded skin and the 21 dps group. (B) Agarose gel electrophoresis confirmed the successful knockout of RMST. (C) QPCR assay showing the expression of RMST 21 dps. (D) H&E and Masson staining of the wounds 21 dps as indicated. (E–F) RMST-KO reduced the (E) thickness and (F) area of neogenic fibrous tissue at 21 dps. (G–H) QPCR showing the COL1A1 and α-SMA levels were significantly decreased in the RMST-KO group compared to the WT group 21 dps. (I) Representative blot of COL1A1 and α-SMA 21 dps. (J–K) Statistical analysis of the immunoblot bands indicated that RMST-KO significantly suppressed the expression of COL1A1 and α-SMA 21 dps. Data were shown as mean ± SD, n = 6, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Il-1β (16806-1-AP) , 1:2000 , Proteintech.

Techniques: Expressing, Agarose Gel Electrophoresis, Knock-Out, Staining, Western Blot

Journal: Biochemistry and Biophysics Reports

Article Title: LncRNA RMST knockout inhibits fibrosis by down-regulating Smad3 during mouse skin wound healing

doi: 10.1016/j.bbrep.2025.102386

Figure Lengend Snippet: RMST-KO reduced the inflammation during mouse skin wound healing. (A–B) QPCR assay showed the mRNA expression of TNF-α and IL-1β were significantly decreased in the RMST-KO group 21 dps. (C) Representative blot of TNF-α, IL-1β 21 dps. (D–E) Statistical analysis of the immunoblot bands indicated that RMST-KO significantly suppressed TNF-α, IL-1β expression 21 dps. Data were shown as mean ± SD, n = 6, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Il-1β (16806-1-AP) , 1:2000 , Proteintech.

Techniques: Expressing, Western Blot

Journal: Biochemistry and Biophysics Reports

Article Title: LncRNA RMST knockout inhibits fibrosis by down-regulating Smad3 during mouse skin wound healing

doi: 10.1016/j.bbrep.2025.102386

Figure Lengend Snippet: Smad3 was a downstream molecule of lncRNA RMST. (A) The heatmap shows the upregulated long non-coding RNAs in the GSE28914 dataset. (B) The catRAPID omics v2.1 software was used to predict the proteins interacting with RMST. (C) A Venn diagram displays the intersection of the two groups of data. (D) GO and KEGG pathway analysis was performed for these 273 intersections.

Article Snippet: Il-1β (16806-1-AP) , 1:2000 , Proteintech.

Techniques: Software

Journal: Biochemistry and Biophysics Reports

Article Title: LncRNA RMST knockout inhibits fibrosis by down-regulating Smad3 during mouse skin wound healing

doi: 10.1016/j.bbrep.2025.102386

Figure Lengend Snippet: Smad3-OE reversed the fibrosis suppression resulting from RMST-KO. (A) QPCR confirmed the upregulating effect of Smad3-OE lentivirus. (B) Representative blot of Smad3 under the effect of Smad3-OE and/or RMST-KO. (C) Statistical analysis of the immunoblot bands. (D) H&E and Masson staining of the wounds as indicated. (E–F) Statistical analysis of the (E) thickness and (F) area of neogenic fibrous tissue 21 dps. (G–I) qPCR detection of fibrosis markers and proteins in classical fibrosis pathways, including COL1, α-SMA, and TGF-β1. (J–M). Representative blot of COL1, α-SMA, and TGF-β1. (N–O) qPCR detection of inflammatory cytokines TNF-α and IL-1β. (P–R) Representative blot of TNF-α and IL-1β. Data were shown as mean ± SD, n = 6, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Il-1β (16806-1-AP) , 1:2000 , Proteintech.

Techniques: Western Blot, Staining

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