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

Journal: International Journal of Nanomedicine

Article Title: Carbon Dots Derived from Ligusticum chuanxiong Alleviate Acute Kidney Injury by Scavenging ROS and Restoring Mitochondrial Homeostasis

doi: 10.2147/IJN.S577611

Figure Lengend Snippet: LC-CDs Preserved Mitochondrial Homeostasis By Suppressing Mitophagy and Apoptosis. ( A ) TUNEL fluorescence staining of renal tissues revealing apoptotic cells across treatment groups (scale bar = 2 mm). ( B ) Representative immunofluorescence images of mitophagy markers (green, LC3-II; red, p62) in renal tissues across experimental groups (scale bar = 50 μm). ( C ) Western blot analysis of apoptosis-related protein (caspase-3) expression in rat kidney tissues in each treatment group. ( D and E ) Western blot analysis of mitophagy-related proteins (LC3-II and p62) in rat kidney tissues in each treatment group. ( F ) Grayscale quantification of caspase-3 expression. ( G and H ) Grayscale quantification of p62 and LC3-II expression. ( I and J ) Corresponding semiquantitative analysis of fluorescence intensity in HK-2 cells. ( K – M ) Representative Western blots of LC3-II, p62, laminA, GAPDH, and VDAC from subfractions of HK-2 cells. Lamin A, GAPDH, and VDAC were used as markers of nuclear, cytosolic, and mitochondrial fractions, respectively. ( N and O ) Molecular docking simulations of L. chuanxiong components with LC3-II and p62. Dashed box highlights interaction interface between the protein receptor ligand and core binding domain, which is critical for predicting binding affinity and stability. Data are presented as means ± SDs. One-way analysis of variance was performed with a post hoc Student–Newman–Keuls test. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Antibodies were obtained from Cell Signaling Technology (USA), including LC3A/B (12741T), cleaved caspase-3 (14220T), and p62/SQSTM1 (5114T).

Techniques: TUNEL Assay, Fluorescence, Staining, Immunofluorescence, Western Blot, Expressing, Binding Assay