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Verification of the therapeutic effect of PM in delaying the senescence of chondrocytes. (a) Schematic diagram of primary chondrocyte isolation and in vitro experimental design. (b) Representative images of brightfield, Alcian blue, Safranin O, and Toluidine blue staining of chondrocytes. (c, d) Protein levels of p16 and SLPI detected by Western blot (WB) <t>after</t> <t>IL-1β</t> treatment (c) or Slpi overexpression (OE-Slpi; d). (e, f) Representative images of SA-β-gal staining (e) and quantitative analysis of positive cells (f) in OE-negative control (OE-NC) or OE-Slpi chondrocytes. (g, h) Representative images of SA-β-gal staining (g) and quantitative analysis of positive cells (h) in chondrocytes treated with 10 ng/ml IL-1β alone or combined with 1 μM PM. (i, j) Quantitative real-time PCR (qPCR) analysis of p16 and MMP3 mRNA expression in chondrocytes treated with 10 ng/ml IL-1β alone or combined with 1 μM PM. (k, l) Representative images of SA-β-gal staining (k) and quantitative analysis of positive cells (l) in chondrocytes treated with H₂O₂ alone or combined with 1 μM PM. (m, n) qPCR analysis of p16 and MMP3 mRNA expression in chondrocytes treated with H₂O₂ alone or combined with 1 μM PM. Data are presented as mean ± standard deviation (n = 3 independent experiments). *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; ns, not significant. (Student’s t -test: f; ANOVA: h, i, j, l, m, n). OE, overexpression; NC, negative control.
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Verification of the therapeutic effect of PM in delaying the senescence of chondrocytes. (a) Schematic diagram of primary chondrocyte isolation and in vitro experimental design. (b) Representative images of brightfield, Alcian blue, Safranin O, and Toluidine blue staining of chondrocytes. (c, d) Protein levels of p16 and SLPI detected by Western blot (WB) <t>after</t> <t>IL-1β</t> treatment (c) or Slpi overexpression (OE-Slpi; d). (e, f) Representative images of SA-β-gal staining (e) and quantitative analysis of positive cells (f) in OE-negative control (OE-NC) or OE-Slpi chondrocytes. (g, h) Representative images of SA-β-gal staining (g) and quantitative analysis of positive cells (h) in chondrocytes treated with 10 ng/ml IL-1β alone or combined with 1 μM PM. (i, j) Quantitative real-time PCR (qPCR) analysis of p16 and MMP3 mRNA expression in chondrocytes treated with 10 ng/ml IL-1β alone or combined with 1 μM PM. (k, l) Representative images of SA-β-gal staining (k) and quantitative analysis of positive cells (l) in chondrocytes treated with H₂O₂ alone or combined with 1 μM PM. (m, n) qPCR analysis of p16 and MMP3 mRNA expression in chondrocytes treated with H₂O₂ alone or combined with 1 μM PM. Data are presented as mean ± standard deviation (n = 3 independent experiments). *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; ns, not significant. (Student’s t -test: f; ANOVA: h, i, j, l, m, n). OE, overexpression; NC, negative control.
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Verification of the therapeutic effect of PM in delaying the senescence of chondrocytes. (a) Schematic diagram of primary chondrocyte isolation and in vitro experimental design. (b) Representative images of brightfield, Alcian blue, Safranin O, and Toluidine blue staining of chondrocytes. (c, d) Protein levels of p16 and SLPI detected by Western blot (WB) <t>after</t> <t>IL-1β</t> treatment (c) or Slpi overexpression (OE-Slpi; d). (e, f) Representative images of SA-β-gal staining (e) and quantitative analysis of positive cells (f) in OE-negative control (OE-NC) or OE-Slpi chondrocytes. (g, h) Representative images of SA-β-gal staining (g) and quantitative analysis of positive cells (h) in chondrocytes treated with 10 ng/ml IL-1β alone or combined with 1 μM PM. (i, j) Quantitative real-time PCR (qPCR) analysis of p16 and MMP3 mRNA expression in chondrocytes treated with 10 ng/ml IL-1β alone or combined with 1 μM PM. (k, l) Representative images of SA-β-gal staining (k) and quantitative analysis of positive cells (l) in chondrocytes treated with H₂O₂ alone or combined with 1 μM PM. (m, n) qPCR analysis of p16 and MMP3 mRNA expression in chondrocytes treated with H₂O₂ alone or combined with 1 μM PM. Data are presented as mean ± standard deviation (n = 3 independent experiments). *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; ns, not significant. (Student’s t -test: f; ANOVA: h, i, j, l, m, n). OE, overexpression; NC, negative control.
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MedChemExpress tgf β1 activator treatment
CD248 knockdown inhibits the activation of TGF-β/Smad signaling pathway in HG-induced HK-2 cells. A & B After transfection with si-NC or si-CD248#1/2, HK-2 cells were treated with normal glucose (NG) or high glucose (HG) for 48 h, and then the protein expression levels of <t>TGF-β1,</t> p-Smad2, p-Smad3, Smad4 ( A ) and p-Smad1/5/9 and Smad7 ( B ) were detected by Western blot. Data were presented as mean ± SD ( n = 3 independent experiments). * P < 0.05, *** P < 0.001
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Image Search Results


Verification of the therapeutic effect of PM in delaying the senescence of chondrocytes. (a) Schematic diagram of primary chondrocyte isolation and in vitro experimental design. (b) Representative images of brightfield, Alcian blue, Safranin O, and Toluidine blue staining of chondrocytes. (c, d) Protein levels of p16 and SLPI detected by Western blot (WB) after IL-1β treatment (c) or Slpi overexpression (OE-Slpi; d). (e, f) Representative images of SA-β-gal staining (e) and quantitative analysis of positive cells (f) in OE-negative control (OE-NC) or OE-Slpi chondrocytes. (g, h) Representative images of SA-β-gal staining (g) and quantitative analysis of positive cells (h) in chondrocytes treated with 10 ng/ml IL-1β alone or combined with 1 μM PM. (i, j) Quantitative real-time PCR (qPCR) analysis of p16 and MMP3 mRNA expression in chondrocytes treated with 10 ng/ml IL-1β alone or combined with 1 μM PM. (k, l) Representative images of SA-β-gal staining (k) and quantitative analysis of positive cells (l) in chondrocytes treated with H₂O₂ alone or combined with 1 μM PM. (m, n) qPCR analysis of p16 and MMP3 mRNA expression in chondrocytes treated with H₂O₂ alone or combined with 1 μM PM. Data are presented as mean ± standard deviation (n = 3 independent experiments). *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; ns, not significant. (Student’s t -test: f; ANOVA: h, i, j, l, m, n). OE, overexpression; NC, negative control.

Journal: Computational and Structural Biotechnology Journal

Article Title: seneR: An R package for comprehensive senescence assessment and its application in type 2 diabetes and osteoarthritis

doi: 10.1016/j.csbj.2025.12.031

Figure Lengend Snippet: Verification of the therapeutic effect of PM in delaying the senescence of chondrocytes. (a) Schematic diagram of primary chondrocyte isolation and in vitro experimental design. (b) Representative images of brightfield, Alcian blue, Safranin O, and Toluidine blue staining of chondrocytes. (c, d) Protein levels of p16 and SLPI detected by Western blot (WB) after IL-1β treatment (c) or Slpi overexpression (OE-Slpi; d). (e, f) Representative images of SA-β-gal staining (e) and quantitative analysis of positive cells (f) in OE-negative control (OE-NC) or OE-Slpi chondrocytes. (g, h) Representative images of SA-β-gal staining (g) and quantitative analysis of positive cells (h) in chondrocytes treated with 10 ng/ml IL-1β alone or combined with 1 μM PM. (i, j) Quantitative real-time PCR (qPCR) analysis of p16 and MMP3 mRNA expression in chondrocytes treated with 10 ng/ml IL-1β alone or combined with 1 μM PM. (k, l) Representative images of SA-β-gal staining (k) and quantitative analysis of positive cells (l) in chondrocytes treated with H₂O₂ alone or combined with 1 μM PM. (m, n) qPCR analysis of p16 and MMP3 mRNA expression in chondrocytes treated with H₂O₂ alone or combined with 1 μM PM. Data are presented as mean ± standard deviation (n = 3 independent experiments). *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; ns, not significant. (Student’s t -test: f; ANOVA: h, i, j, l, m, n). OE, overexpression; NC, negative control.

Article Snippet: For over-expression SLPI, chondrocytes were transfected with pcDNA3.1/Slpi full-length plasmid using Lipo8000 (Beyotime) according to the manufacturer’s instructions.For IL-1β treatment, mouse primary chondrocytes were treated with recombinant mouse IL-1β (10 ng/ml, MedChemExpress) for 24 h. For H2O2-induced senescence, mouse primary chondrocytes were treated with H2O2 (200 μM, MKBio Shanghai) for 2 h. For PM treatment, mouse primary chondrocytes were treated with or without PM (MedChemExpress), dissolved in DMSO (Dimethyl sulfoxide, MedChemExpress).

Techniques: Isolation, In Vitro, Staining, Western Blot, Over Expression, Negative Control, Real-time Polymerase Chain Reaction, Expressing, Standard Deviation

CD248 knockdown inhibits the activation of TGF-β/Smad signaling pathway in HG-induced HK-2 cells. A & B After transfection with si-NC or si-CD248#1/2, HK-2 cells were treated with normal glucose (NG) or high glucose (HG) for 48 h, and then the protein expression levels of TGF-β1, p-Smad2, p-Smad3, Smad4 ( A ) and p-Smad1/5/9 and Smad7 ( B ) were detected by Western blot. Data were presented as mean ± SD ( n = 3 independent experiments). * P < 0.05, *** P < 0.001

Journal: Hereditas

Article Title: CD248, targeted by veratramine and neobavaisoflavone, mediates pathological changes of renal tubular epithelial cells induced by high glucose

doi: 10.1186/s41065-025-00624-z

Figure Lengend Snippet: CD248 knockdown inhibits the activation of TGF-β/Smad signaling pathway in HG-induced HK-2 cells. A & B After transfection with si-NC or si-CD248#1/2, HK-2 cells were treated with normal glucose (NG) or high glucose (HG) for 48 h, and then the protein expression levels of TGF-β1, p-Smad2, p-Smad3, Smad4 ( A ) and p-Smad1/5/9 and Smad7 ( B ) were detected by Western blot. Data were presented as mean ± SD ( n = 3 independent experiments). * P < 0.05, *** P < 0.001

Article Snippet: For TGF-β1 activator treatment, HK-2 cells were pretreated with SRI-011381 hydrochloride (10 μM; MedChemExpress, Shanghai, China) [ ] for 2 h, then transfected with si-CD248#1 or si-NC, and finally treated with HG for 48 h. VER (purity > 98%) and NBIF (purity: 99.91%) were purchased from MedChemExpress (Shanghai, China).

Techniques: Knockdown, Activation Assay, Transfection, Expressing, Western Blot

Effect of VER or NBIF treatment on TGF-β/Smad axis in HG-induced HK-2 cells. A & B HK-2 cells were pretreated with 10 µM and 20 µM VER ( A ) or 10 µM and 40 µM NBIF ( B ) for 24 h and then treated with normal glucose (NG) or high glucose (HG) for 48 h. The protein expression levels of CD248, TGF-β1, p-Smad2, p-Smad3 and Smad4 in HK-2 cells were then detected by Western blot. Data were presented as mean ± SD ( n = 3 independent experiments). * P < 0.05, ** P < 0.01, and *** P < 0.001

Journal: Hereditas

Article Title: CD248, targeted by veratramine and neobavaisoflavone, mediates pathological changes of renal tubular epithelial cells induced by high glucose

doi: 10.1186/s41065-025-00624-z

Figure Lengend Snippet: Effect of VER or NBIF treatment on TGF-β/Smad axis in HG-induced HK-2 cells. A & B HK-2 cells were pretreated with 10 µM and 20 µM VER ( A ) or 10 µM and 40 µM NBIF ( B ) for 24 h and then treated with normal glucose (NG) or high glucose (HG) for 48 h. The protein expression levels of CD248, TGF-β1, p-Smad2, p-Smad3 and Smad4 in HK-2 cells were then detected by Western blot. Data were presented as mean ± SD ( n = 3 independent experiments). * P < 0.05, ** P < 0.01, and *** P < 0.001

Article Snippet: For TGF-β1 activator treatment, HK-2 cells were pretreated with SRI-011381 hydrochloride (10 μM; MedChemExpress, Shanghai, China) [ ] for 2 h, then transfected with si-CD248#1 or si-NC, and finally treated with HG for 48 h. VER (purity > 98%) and NBIF (purity: 99.91%) were purchased from MedChemExpress (Shanghai, China).

Techniques: Expressing, Western Blot

VER and NBIF alleviates inflammation, ECM deposition, and inhibits the activation of the TGF-β1/Smad pathway in db/db mice. A - D The mRNA expression levels of TNF-α, IL-6, IL-1β, and CD248 in the kidney tissues of the animals in different groups were detected by qPCR. E - H The protein levels of CD248, ECM proteins (α-SMA, Collagen I/IV, Fibronectin), and TGF-β1/Smad pathway-related molecules in the kidney tissues of the animals in different groups were detected by Western blot. Data are presented as mean ± SD, n = 6. * P < 0.05, ** P < 0.01, and *** P < 0.001

Journal: Hereditas

Article Title: CD248, targeted by veratramine and neobavaisoflavone, mediates pathological changes of renal tubular epithelial cells induced by high glucose

doi: 10.1186/s41065-025-00624-z

Figure Lengend Snippet: VER and NBIF alleviates inflammation, ECM deposition, and inhibits the activation of the TGF-β1/Smad pathway in db/db mice. A - D The mRNA expression levels of TNF-α, IL-6, IL-1β, and CD248 in the kidney tissues of the animals in different groups were detected by qPCR. E - H The protein levels of CD248, ECM proteins (α-SMA, Collagen I/IV, Fibronectin), and TGF-β1/Smad pathway-related molecules in the kidney tissues of the animals in different groups were detected by Western blot. Data are presented as mean ± SD, n = 6. * P < 0.05, ** P < 0.01, and *** P < 0.001

Article Snippet: For TGF-β1 activator treatment, HK-2 cells were pretreated with SRI-011381 hydrochloride (10 μM; MedChemExpress, Shanghai, China) [ ] for 2 h, then transfected with si-CD248#1 or si-NC, and finally treated with HG for 48 h. VER (purity > 98%) and NBIF (purity: 99.91%) were purchased from MedChemExpress (Shanghai, China).

Techniques: Activation Assay, Expressing, Western Blot