p62  (Tanabe)

Journal: Scientific Reports

Article Title: Dapagliflozin attenuates cisplatin-induced nephrotoxicity in rats through modulation of ROS/NF-κB, BCL2/Bax and PINK1/Parkin signaling pathways

doi: 10.1038/s41598-026-50755-0

Figure Lengend Snippet: Effects of dapagliflozin pretreatment on mitophagy and autophagy markers in cisplatin-treated rats. The protein expression of ( a ) PTEN-induced kinase 1 (PINK1), ( b ) Parkin, ( c ) Translocase of inner mitochondrial membrane 23 (TIMM23), ( d ) Translocase of outer mitochondrial membrane 20 (TOMM20), ( e ) microtubule-associated protein 1 light chain 3 (LC3)-II, ( f ) LC3II/I ratio and ( g ) p62 in kidney tissues of rats were measured using ELISA. ( h ) Quantification of immunostaining of p62 from the images in ( i ) (× 400), scale bar = 20 µm. All the data were represented as mean ± SD (n = 6). Normal control, NC; Cisplatin, CIS; and Cisplatin + Dapagliflozin, CIS + DPG groups. Statistical analysis was attained using one-way analysis of variance (ANOVA), followed by Tukey–Kramer multiple comparison; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001).

Article Snippet: After blocking, the primary monoclonal antibodies against cleaved caspase-3 (cat# GB11532) (ServiceBio, China) and p62 (cat# bs-2935R) (Bioss, USA) (at a dilution of 1:100) were incubated 30 min with the tissue sections for immunostaining.

Techniques: Expressing, Membrane, Enzyme-linked Immunosorbent Assay, Immunostaining, Control, Comparison

Journal: Bioactive Materials

Article Title: Near infrared enhanced palladium loaded siraitia grosvenorii carbon dots amplify mitophagy for acute lung injury immunotherapy

doi: 10.1016/j.bioactmat.2026.02.040

Figure Lengend Snippet: ALI therapeutic mechanism. A) Co-immunofluorescent staining images of cells incubated with Cy5-CPs or Cy5-CPs@SS31 by confocal staining microscope: DAPI (blue), Mito-tracker green (green), and Cy5-CPs or Cy5-CPs@SS31 (red). (Scale bar = 10 μm) B) MMP of treated cells by flow cytometry. C) Heatmap of DEGs between control group and CPs@SS31+NIR: genes with relatively high (red) and low (blue) expression levels. D) Volcano plot of DEGs: 542 upregulated and 499 downregulated genes between control group and CPs@SS31+NIR. E) Anti-inflammation pathways related DEGs by KEGG enrichment analysis (red). F) Anti-inflammation pathways related differential biological functions by GO enrichment analysis (red): molecular function (MF), biological process (BP) and cell component (CC). G) Protein-protein interaction network of mitophagy related proteins. H) P62, Parkin and PINK1 expression levels of treated cells by WB. I) P62, Parkin and PINK1 expression levels in the lung tissue of treated rats. (Scale bar = 100 μm).

Article Snippet: Furthermore, the membranes were separately incubated with the primary antibody (anti-P62, Parkin, PINK1 and GAPDH, Proteintech, China) overnight at 4 °C.

Techniques: Staining, Incubation, Microscopy, Flow Cytometry, Control, Expressing

Journal: Bioactive Materials

Article Title: A foam cell-targeted lipophagy restoration strategy stabilizes vulnerable atherosclerotic plaques

doi: 10.1016/j.bioactmat.2026.02.041

Figure Lengend Snippet: In vitro evaluation of foam cell lipid accumulation and lipophagy activation following OPN-HMCN@MLT treatment. ( A - C ) ORO and BODIPY staining images and corresponding quantification of ORO and BODIPY positive areas of RAW264.7 cells under different stimulations (n = 5, scale bar for ORO: 100 μm, scale bar for BODIPY: 20 μm). ( D ) Bio-TEM images of RAW264.7 cells post various treatments (n = 5, scale bars 1.0 μm). Green arrows indicate nanoparticles. ( E , F ) Morphometric analysis determined the mean number and area (μm 2 ) of LDs per cell section. ( G ) Confocal images depicting lipophagy flux in foam cells following different treatments (n = 5 biological replicates, scale bars: 10 μm). ( H - J ) The quantities of acidified autophagosomes (GFP-RFP+), neutral autophagosomes (GFP + RFP+), and LDs labeled with BODIPY were measured per cell for each condition. (K to N) Representative Western blot images and quantitative analysis of LC3, LAMP1, and P62 expression in foam cells. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.

Article Snippet: To block nonspecific binding, membranes were incubated with 5% skim milk for 1 h. Thereafter, membranes were incubated overnight at 4 °C with primary antibodies against ABCA1, ABCG1, ACOX1, CPT1A, LC3 (ab192890, 1:2000, abcam), LAMP1 (84658-5-RR, 1:8000, Proteintech), PPARα (66826-1-Ig, 1:3000, Proteintech), PPARγ (66936-1-Ig, 1:10000, Proteintech), P62 (18420-1-AP, 1:10000, Proteintech), MCAD (55210-1-AP, 1:3000, Proteintech), LCAD (17526-1-AP, 1:10000, Proteintech), tubulin (80762-1-RR, 1:10000, Proteintech), GAPDH (60004-1-Ig, 1:50000, Proteintech), and β-actin (66009-1-Ig, 1:20000, Proteintech).

Techniques: In Vitro, Activation Assay, Staining, Labeling, Western Blot, Expressing

Journal: Oncology Reports

Article Title: Platycodin D sensitizes head and neck squamous cell carcinoma to cisplatin by inducing autophagy arrest

doi: 10.3892/or.2026.9088

Figure Lengend Snippet: PD and cisplatin combination treatment increases autophagy marker levels in head and neck squamous cell carcinoma cells. (A) HSC3 and (C) FaDu cells were treated with PD (10 µM), cisplatin (10 µM) or combination treatment for 48 h. Cells were stained with LC3B antibody and analyzed using confocal microscopy. (B) In HSC3 cells, p62 immunofluorescence was increased following combination treatment compared with single treatments. (D) In FaDu cells, p62 staining similarly showed higher p62 levels in the combination treatment group than in the single treatment groups. Nuclei were stained with DAPI (blue), LC3B was stained red and p62 was stained green. Fluorescence intensity and puncta quantification were analyzed using ZEN software (Zeiss AG). Scale bar, 50 µm. Data are presented as the mean ± SD (n=3). *P<0.05, **P<0.01, ***P<0.001. PD, Platycodin D.

Article Snippet: The following antibodies were used: Anti-LC3A/B (1:1,000; cat. no. 12741S; Cell Signaling Technology, Inc.), anti-SQSTM1/p62 (1:1,000; cat. no. 5114S; Cell Signaling Technology, Inc.), anti-poly(ADP-ribose) polymerase (PARP; 1:1,000; cat. no. 9542S; Cell Signaling Technology, Inc.), anti-caspase 3 (1:1,000; cat. no. 9662S; Cell Signaling Technology, Inc.) and anti-β-actin (1:5,000; cat. no. 47778; Santa Cruz Biotechnology, Inc.).

Techniques: Marker, Staining, Confocal Microscopy, Immunofluorescence, Fluorescence, Software

Journal: Oncology Reports

Article Title: Platycodin D sensitizes head and neck squamous cell carcinoma to cisplatin by inducing autophagy arrest

doi: 10.3892/or.2026.9088

Figure Lengend Snippet: PD and cisplatin combination treatment induces autophagy arrest by inhibiting autophagosome degradation. HSC3 and FaDu cells were treated with PD (10 µM), cisplatin (10 µM) or combination treatment for 48 h, with or without BafA1. (A) Western blotting was performed to evaluate the expression levels of LC3A/B and p62. β-actin was used as a loading control. (B) Densitometric analysis of LC3A/B and p62 protein levels normalized to β-actin, performed using ImageJ software. Statistical significance was determined by one-way ANOVA followed by Tukey's post hoc test. Data are presented as the mean ± SD (n=3). *P<0.05, **P<0.01. BafA1, Bafilomycin A1; PD, Platycodin D.

Article Snippet: The following antibodies were used: Anti-LC3A/B (1:1,000; cat. no. 12741S; Cell Signaling Technology, Inc.), anti-SQSTM1/p62 (1:1,000; cat. no. 5114S; Cell Signaling Technology, Inc.), anti-poly(ADP-ribose) polymerase (PARP; 1:1,000; cat. no. 9542S; Cell Signaling Technology, Inc.), anti-caspase 3 (1:1,000; cat. no. 9662S; Cell Signaling Technology, Inc.) and anti-β-actin (1:5,000; cat. no. 47778; Santa Cruz Biotechnology, Inc.).

Techniques: Western Blot, Expressing, Control, Software

Journal: Oncology Reports

Article Title: Platycodin D sensitizes head and neck squamous cell carcinoma to cisplatin by inducing autophagy arrest

doi: 10.3892/or.2026.9088

Figure Lengend Snippet: PD and cisplatin combination treatment increases autophagy marker levels in head and neck squamous cell carcinoma cells. (A) HSC3 and (C) FaDu cells were treated with PD (10 µM), cisplatin (10 µM) or combination treatment for 48 h. Cells were stained with LC3B antibody and analyzed using confocal microscopy. (B) In HSC3 cells, p62 immunofluorescence was increased following combination treatment compared with single treatments. (D) In FaDu cells, p62 staining similarly showed higher p62 levels in the combination treatment group than in the single treatment groups. Nuclei were stained with DAPI (blue), LC3B was stained red and p62 was stained green. Fluorescence intensity and puncta quantification were analyzed using ZEN software (Zeiss AG). Scale bar, 50 µm. Data are presented as the mean ± SD (n=3). *P<0.05, **P<0.01, ***P<0.001. PD, Platycodin D.

Article Snippet: The cells were incubated overnight at 4°C with primary antibodies against LC3B (1:1,000; cat. no. 2775S; Cell Signaling Technology, Inc.) and sequestosome 1 (SQSTM1)/p62 (1:1,000; cat. no. 5114S; Cell Signaling Technology, Inc.).

Techniques: Marker, Staining, Confocal Microscopy, Immunofluorescence, Fluorescence, Software

Journal: Oncology Reports

Article Title: Platycodin D sensitizes head and neck squamous cell carcinoma to cisplatin by inducing autophagy arrest

doi: 10.3892/or.2026.9088

Figure Lengend Snippet: PD and cisplatin combination treatment induces autophagy arrest by inhibiting autophagosome degradation. HSC3 and FaDu cells were treated with PD (10 µM), cisplatin (10 µM) or combination treatment for 48 h, with or without BafA1. (A) Western blotting was performed to evaluate the expression levels of LC3A/B and p62. β-actin was used as a loading control. (B) Densitometric analysis of LC3A/B and p62 protein levels normalized to β-actin, performed using ImageJ software. Statistical significance was determined by one-way ANOVA followed by Tukey's post hoc test. Data are presented as the mean ± SD (n=3). *P<0.05, **P<0.01. BafA1, Bafilomycin A1; PD, Platycodin D.

Article Snippet: The cells were incubated overnight at 4°C with primary antibodies against LC3B (1:1,000; cat. no. 2775S; Cell Signaling Technology, Inc.) and sequestosome 1 (SQSTM1)/p62 (1:1,000; cat. no. 5114S; Cell Signaling Technology, Inc.).

Techniques: Western Blot, Expressing, Control, Software