Journal: Biology Direct

Article Title: Polydatin mitigates cigarette smoke-induced pulmonary apoptosis by regulating Bim via FoxO3 post-translational modifications and modulating the gut microenvironment

doi: 10.1186/s13062-026-00924-y

Figure Lengend Snippet: Schematic representation of polydatin and the animal experimental workflow. ( A ) Molecular structure of polydatin. ( B ) Chronological overview of the in vivo study design and experimental procedure

Article Snippet: Polydatin (Fig. A) and GDC-0068 were procured from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: In Vivo

Journal: Biology Direct

Article Title: Polydatin mitigates cigarette smoke-induced pulmonary apoptosis by regulating Bim via FoxO3 post-translational modifications and modulating the gut microenvironment

doi: 10.1186/s13062-026-00924-y

Figure Lengend Snippet: Polydatin attenuates CSE-induced pulmonary pathology, oxidative stress, and the inflammatory response in a murine model. ( A ) Schematic illustration outlining the treatment regimens across the five experimental cohorts. ( B ) Terminal body weights of mice in each group recorded at the conclusion of the study ( n = 6). ( C ) Pulmonary index assessment ( n = 6). ( D ) Serum concentrations of malondialdehyde ( n = 3). ( E ) Superoxide dismutase enzymatic activity within lung homogenates ( n = 3). ( F ) Relative mRNA abundance of pro-inflammatory indicators (Il1b, Il6) and the pro-apoptotic factor (Bax) in lung tissues ( n = 3). ( G ) Representative photomicrographs of H&E-stained pulmonary sections ( n = 3). Scale bar, 100 μm. ( H, I ) Representative WB profiles and the associated densitometric quantification of pivotal inflammatory protein markers in lung tissues( n = 3). *p < 0.05, **p < 0.01, ***p < 0.001 vs. CSE group. Data are expressed as mean ± standard deviation (SD)

Article Snippet: Polydatin (Fig. A) and GDC-0068 were procured from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Pathology, Activity Assay, Staining, Standard Deviation

Journal: Biology Direct

Article Title: Polydatin mitigates cigarette smoke-induced pulmonary apoptosis by regulating Bim via FoxO3 post-translational modifications and modulating the gut microenvironment

doi: 10.1186/s13062-026-00924-y

Figure Lengend Snippet: Transcriptomic profiling elucidates the FoxO and apoptosis cascades as pivotal regulatory targets of polydatin in pulmonary tissues. ( A ) Hierarchical clustering heatmap of differentially expressed genes (DEGs) in lung tissues across the Control, Model, and Pol40 (40 mg/kg polydatin) cohorts ( n = 3 per group). ( B ) Gene Set Enrichment Analysis (GSEA) profiles demonstrating the statistically significant enrichment of chemokine signaling and apoptosis-related gene sets among the treatment cohorts. ( C ) Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of DEGs, underscoring the prominent modulation of the FoxO signaling cascade. ( D ) Gene Ontology (GO) functional enrichment analysis

Article Snippet: Polydatin (Fig. A) and GDC-0068 were procured from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Profiling, Control, Analysis, Functional Assay

Journal: Biology Direct

Article Title: Polydatin mitigates cigarette smoke-induced pulmonary apoptosis by regulating Bim via FoxO3 post-translational modifications and modulating the gut microenvironment

doi: 10.1186/s13062-026-00924-y

Figure Lengend Snippet: Polydatin activates AKT1/FoxO3 signaling via direct binding to AKT1. ( A ) Molecular docking analysis of polydatin binding to the AKT1 activation loop (T308). ( B-C ) WB ( B ) and quantification ( C ) of total and P-AKT1 (Thr308) and FoxO3 (Ser253) in lung tissues( n = 3). ( D ) Immunofluorescence co-staining of P-AKT1 (Thr308) and FoxO3 in pulmonary alveoli. Scale bar, 50 μm. *p < 0.05, **p < 0.01, ***p < 0.001 vs. CSE group. Data are expressed as mean ± standard deviation (SD)

Article Snippet: Polydatin (Fig. A) and GDC-0068 were procured from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Binding Assay, Docking Assay, Analysis, Activation Assay, Immunofluorescence, Staining, Standard Deviation

Journal: Biology Direct

Article Title: Polydatin mitigates cigarette smoke-induced pulmonary apoptosis by regulating Bim via FoxO3 post-translational modifications and modulating the gut microenvironment

doi: 10.1186/s13062-026-00924-y

Figure Lengend Snippet: Polydatin inhibits CSE-induced Bim expression. ( A ) Immunofluorescence staining of Bim in alveolar septa. Scale bar, 50 μm. ( B ) Heatmap illustrating mRNA expression levels (FPKM) of Bim, Bax, and Bcl-2 from transcriptomic profiling ( n = 3). ( C–D ) Western blot ( C ) and quantification ( D ) of Bim protein levels in lung tissues ( n = 3). *p < 0.05, **p < 0.01, ***p < 0.001 vs. CSE group. Data are expressed as mean ± standard deviation (SD)

Article Snippet: Polydatin (Fig. A) and GDC-0068 were procured from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Expressing, Immunofluorescence, Staining, Profiling, Western Blot, Standard Deviation

Journal: Biology Direct

Article Title: Polydatin mitigates cigarette smoke-induced pulmonary apoptosis by regulating Bim via FoxO3 post-translational modifications and modulating the gut microenvironment

doi: 10.1186/s13062-026-00924-y

Figure Lengend Snippet: Polydatin attenuates CSE-induced lung apoptosis. ( A ) TUNEL staining of lung sections. Scale bar, 50 μm. ( B–C ) Western blot ( B ) and quantification ( C ) of pro-apoptotic (Bax, Cleaved-Caspase 3) and anti-apoptotic (Bcl-2) proteins ( n = 3). *p < 0.05, **p < 0.01, ***p < 0.001 vs. CSE group. Data are expressed as mean ± standard deviation (SD)

Article Snippet: Polydatin (Fig. A) and GDC-0068 were procured from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: TUNEL Assay, Staining, Western Blot, Standard Deviation

Journal: Biology Direct

Article Title: Polydatin mitigates cigarette smoke-induced pulmonary apoptosis by regulating Bim via FoxO3 post-translational modifications and modulating the gut microenvironment

doi: 10.1186/s13062-026-00924-y

Figure Lengend Snippet: Polydatin regulates Bim expression via the AKT-FoxO3 axis in MLE12 cells. ( A-C ) WB and quantification of AKT, P-AKT (Thr308), FoxO3a, P-FoxO3a (Ser253) and Bim in MLE12 cells treated with CSE and varying concentrations of polydatin ( n = 3). ( D–E ) WB and quantification showing the effects of SC79 (AKT activator) and GDC-0068 (AKT inhibitor) ( n = 3). *p < 0.05, **p < 0.01, ***p < 0.001 vs. CSE group. Data are expressed as mean ± standard deviation (SD)

Article Snippet: Polydatin (Fig. A) and GDC-0068 were procured from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Expressing, Standard Deviation

Journal: Biology Direct

Article Title: Polydatin mitigates cigarette smoke-induced pulmonary apoptosis by regulating Bim via FoxO3 post-translational modifications and modulating the gut microenvironment

doi: 10.1186/s13062-026-00924-y

Figure Lengend Snippet: Polydatin regulates FoxO3 nucleocytoplasmic translocation in an AKT-dependent manner. ( A ) Representative immunofluorescence images of FoxO3 localization in MLE12 cells. Scale bar, 50 μm. ( B–C ) WB and quantification of FoxO3 levels in nuclear and cytoplasmic fractions ( n = 3). *p < 0.05, **p < 0.01, ***p < 0.001 vs. CSE group. Data are expressed as mean ± standard deviation (SD)

Article Snippet: Polydatin (Fig. A) and GDC-0068 were procured from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Translocation Assay, Immunofluorescence, Standard Deviation

Journal: Biology Direct

Article Title: Polydatin mitigates cigarette smoke-induced pulmonary apoptosis by regulating Bim via FoxO3 post-translational modifications and modulating the gut microenvironment

doi: 10.1186/s13062-026-00924-y

Figure Lengend Snippet: Polydatin modulates the intestinal metabolic profile in CSE-exposed mice. ( A ) Heatmap and cluster analysis of intestinal metabolites based on untargeted metabolomics ( n = 3). ( B ) Proportional distribution of differential metabolites. ( C ) Volcano visualization of significant metabolite alterations in the intergroup comparison. ( D ) Bar chart of significantly altered intestinal metabolites. ( E ) Bubble diagram of KEGG pathway enrichment analysis based on intergroup differential metabolites

Article Snippet: Polydatin (Fig. A) and GDC-0068 were procured from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Analysis, Comparison

Journal: Biology Direct

Article Title: Polydatin mitigates cigarette smoke-induced pulmonary apoptosis by regulating Bim via FoxO3 post-translational modifications and modulating the gut microenvironment

doi: 10.1186/s13062-026-00924-y

Figure Lengend Snippet: Polydatin restores intestinal microbiota diversity and maintains colonic barrier integrity in CSE-exposed mice. ( A ) Alpha diversity assessed by the Chao1 index ( n = 3). ( B ) Beta diversity visualized via Partial Least Squares Discriminant Analysis (PLS-DA) ( n = 3). ( C ) Comparative analysis of intestinal bactirium-spectrum across groups at the family and genus levels. ( D-E ) Relative abundance of differential microbial genera in colonic mucosa based on Wilcoxon rank-sum tests ( n = 3). ( F ) Representative H&E-stained images and immunohistochemical staining of ZO-1/Occludin in intestinal tissues ( n = 3). Scale bar, 100 μm

Article Snippet: Polydatin (Fig. A) and GDC-0068 were procured from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Analysis, Staining, Immunohistochemical staining

Journal: Biology Direct

Article Title: Polydatin mitigates cigarette smoke-induced pulmonary apoptosis by regulating Bim via FoxO3 post-translational modifications and modulating the gut microenvironment

doi: 10.1186/s13062-026-00924-y

Figure Lengend Snippet: Graphical abstract illustrating the mechanisms by which polydatin mitigates cigarette smoke-induced pulmonary inflammation and apoptosis by modulating the gut microenvironment and regulating Bim via FoxO3 post-translational modifications

Article Snippet: Polydatin (Fig. A) and GDC-0068 were procured from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques:

Journal: MethodsX

Article Title: An accessible HPLC-DAD method for the direct detection of acrolein-trapping compounds in complex plant matrices ☆

doi: 10.1016/j.mex.2025.103747

Figure Lengend Snippet: Chromatographic profile of the ten-component mixture, with detection at a wavelength of 280 nm. The upper chromatogram corresponds to the negative control (0 mM acrolein), while the lower chromatogram represents the mixture following pretreatment with 5 mM acrolein. 1: protocatechuic acid, 2: esculin, 3: catechin, 4: epicatechin, 5: coumaric acid, 6: piceid, 7: rutin, 8: phloridzin, 9: resveratrol, 10: phloretin. Acrolein-trapping compounds are highlighted in red.

Article Snippet: 2,4-Dinitrophenylhydrazine hydrochloride (DNPH), aminoguanidine hydrochloride, esculin, piceid and phloretin were obtained from TCI Chemicals.

Techniques: Negative Control

Journal: Animal Models and Experimental Medicine

Article Title: Polydatin alleviates mitochondrial damage and apoptosis of lung epithelial cells by inhibiting toll‐like receptor 4‐dependent macrophage activation in asthma

doi: 10.1002/ame2.70100

Figure Lengend Snippet: Polydatin relieves ROS (reactive oxygen species) and inflammation in asthmatic mice. To investigate asthma pathology, we developed an asthma mouse model via sensitization of BALB/c mice with ovalbumin (OVA). After initial OVA exposure, animals received intraperitoneal injections of polydatin prior to subsequent aerosolized OVA challenges. (A) Structural representation of polydatin. (B) Experimental protocol diagram illustrating timeline and treatment schedules. (C) Lung resistance alterations in response to methacholine stimulation ( n = 8 per group). (D) Quantification of eosinophils (identified as CD45.2 + Siglec‐F + cells) within bronchoalveolar lavage fluid (BALF) using flow cytometry. (E) Representative histological lung sections stained with hematoxylin–eosin (HE) and periodic acid–Schiff (PAS). (F) Measurement of cytokine concentrations in BALF using ELISA (enzyme‐linked immunosorbent assay) assays ( n = 8 per group). (G) Fluorescent microscopic images demonstrating ROS (reactive oxygen species) production via dihydroethidium (DHE) staining in lung tissues. (H) WB (Western blotting) quantification of NOX2 (NADPH oxidase 2) and NOX4 (NADPH oxidase 4) protein expression in pulmonary tissues. (I) Identification of apoptotic cells using TUNEL (terminal deoxynucleotidyl transferase dUTP nick‐end labeling) staining in lung sections with corresponding quantitative analysis of positive cells ( n = 3). (J) WB detection of apoptosis‐related proteins within lung homogenates. (K) Immunohistochemical staining depicting the expression and localization of cleaved caspase‐3 and cleaved caspase‐9 proteins ( n = 3). * p < 0.05, ** p < 0.01, and *** p < 0.001.

Article Snippet: Prior to LPS and ATP stimulation, cells were pretreated for 1 h with polydatin (50 or 100 μmol/L), CLI‐095 (a TLR4‐specific inhibitor, CAS: 243984‐11‐4, 1 μg/mL, InvivoGen), or A438079 (a P2X7R‐specific antagonist, CAS: 899507‐36‐9, 10 μmol/L, Abcam).

Techniques: Flow Cytometry, Staining, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, TUNEL Assay, Immunohistochemical staining

Journal: Animal Models and Experimental Medicine

Article Title: Polydatin alleviates mitochondrial damage and apoptosis of lung epithelial cells by inhibiting toll‐like receptor 4‐dependent macrophage activation in asthma

doi: 10.1002/ame2.70100

Figure Lengend Snippet: Polydatin suppresses TLR4 (toll‐like receptor 4)/P2X7R/NLRP3 (NOD‐like receptor protein) activation in OVA (ovalbumin)–induced asthma. WB (Western blotting) measured (A) TLR4, IκBα, NF‐κB (nuclear factor kappa B) P65, and phosphorylation of IκBα and NF‐κB P65, and (B) P2X7R, NLRP3, ASC, and caspase‐1 in lung tissues. (C) Co‐expression of F4/80 (green) and (D) P2X7R (green) with TLR4 (red) in mouse lung tissues was assessed via immunofluorescence staining combined ( n = 3). (E) ELISA (enzyme‐linked immunosorbent assay) and real‐time PCR (polymerase chain reaction) were used to measure IL‐1β (interleukin‐1β) and IL‐18 protein levels in BALF (bronchoalveolar lavage fluid) and mRNA (messenger RNA) expression ( n = 8), and Dunnett's post hoc test (A–D) or Wilcoxon rank‐sum test (E) was performed subsequently. * p < 0.05 and ** p < 0.01.

Article Snippet: Prior to LPS and ATP stimulation, cells were pretreated for 1 h with polydatin (50 or 100 μmol/L), CLI‐095 (a TLR4‐specific inhibitor, CAS: 243984‐11‐4, 1 μg/mL, InvivoGen), or A438079 (a P2X7R‐specific antagonist, CAS: 899507‐36‐9, 10 μmol/L, Abcam).

Techniques: Activation Assay, Western Blot, Phospho-proteomics, Expressing, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction, Polymerase Chain Reaction, RNA Expression

Journal: Animal Models and Experimental Medicine

Article Title: Polydatin alleviates mitochondrial damage and apoptosis of lung epithelial cells by inhibiting toll‐like receptor 4‐dependent macrophage activation in asthma

doi: 10.1002/ame2.70100

Figure Lengend Snippet: Polydatin inhibits IL‐1β (interleukin‐1β) and IL‐18 by blocking the TLR4 (toll‐like receptor 4)/P2X7R pathway in macrophages. (A) Intracellular calcium concentrations were analyzed utilizing Fluo 3‐AM fluorescent staining ( n = 3). (B) WB (Western blotting) was performed to quantify the levels of TLR4, IκBα, NF‐κB (nuclear factor kappa B) p65, phosphorylated forms of IκBα and NF‐κB p65, P2X7R, NLRP3 (NOD‐like receptor protein) inflammasome components, IL‐1β, and IL‐18 ( n = 3). (C) Macrophage‐derived protein secretion levels of IL‐1β and IL‐18 were evaluated using ELISA (enzyme‐linked immunosorbent assay). (A and B) or Wilcoxon rank‐sum testing (C). * p < 0.05 and ** p < 0.01.

Article Snippet: Prior to LPS and ATP stimulation, cells were pretreated for 1 h with polydatin (50 or 100 μmol/L), CLI‐095 (a TLR4‐specific inhibitor, CAS: 243984‐11‐4, 1 μg/mL, InvivoGen), or A438079 (a P2X7R‐specific antagonist, CAS: 899507‐36‐9, 10 μmol/L, Abcam).

Techniques: Blocking Assay, Staining, Western Blot, Derivative Assay, Enzyme-linked Immunosorbent Assay

Journal: Animal Models and Experimental Medicine

Article Title: Polydatin alleviates mitochondrial damage and apoptosis of lung epithelial cells by inhibiting toll‐like receptor 4‐dependent macrophage activation in asthma

doi: 10.1002/ame2.70100

Figure Lengend Snippet: Polydatin suppresses ROS (reactive oxygen species) production and apoptosis of ECs (epithelial cells) by blockage of the TLR4 (toll‐like receptor 4)/P2X7R pathway in macrophages. (A) Intracellular ROS levels in BEAS‐2B cells were determined through DCFH‐DA fluorescence staining (10 μmol/L). (B) Alterations in MMP (mitochondrial membrane potential) were assessed using JC‐1 dye staining. (C) WB (Western blotting) analysis quantified protein expression of NOX2 (NADPH oxidase 2) and NOX4 (NADPH oxidase 4), and proteins related to apoptosis in BEAS‐2B ECs (epithelial cells). (D) Flow cytometry quantified apoptosis based on the proportion of annexin‐V + /7‐AAD + positive cells ( n = 3). (E) Additionally, WB was used to determine apoptosis‐related protein levels in BEAS‐2B cells. Histogram results represent the mean ± SEM (standard error of the mean) from three independent replicates. * p < 0.05 and ** p < 0.01.

Article Snippet: Prior to LPS and ATP stimulation, cells were pretreated for 1 h with polydatin (50 or 100 μmol/L), CLI‐095 (a TLR4‐specific inhibitor, CAS: 243984‐11‐4, 1 μg/mL, InvivoGen), or A438079 (a P2X7R‐specific antagonist, CAS: 899507‐36‐9, 10 μmol/L, Abcam).

Techniques: Fluorescence, Staining, Membrane, Western Blot, Expressing, Flow Cytometry

Journal: Animal Models and Experimental Medicine

Article Title: Polydatin alleviates mitochondrial damage and apoptosis of lung epithelial cells by inhibiting toll‐like receptor 4‐dependent macrophage activation in asthma

doi: 10.1002/ame2.70100

Figure Lengend Snippet: Schematic diagram of the mechanisms underlying the alleviation of OVA (ovalbumin)–induced asthma by polydatin. The alleviation of asthma by polydatin is dependent on the blockage of the TLR4 (toll‐like receptor 4)/P2X7R synergy in macrophages. The blockage of the TLR4/P2X7R synergy results in decreased release and secretion of IL‐1β (interleukin‐1β) and IL‐18In ECs, low IL‐1β and IL‐18 levels inhibit mitochondrial damage and apoptosis.

Article Snippet: Prior to LPS and ATP stimulation, cells were pretreated for 1 h with polydatin (50 or 100 μmol/L), CLI‐095 (a TLR4‐specific inhibitor, CAS: 243984‐11‐4, 1 μg/mL, InvivoGen), or A438079 (a P2X7R‐specific antagonist, CAS: 899507‐36‐9, 10 μmol/L, Abcam).

Techniques:

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Lactate-driven lactylation of HNRNPA1 orchestrates PKM2 splicing and glycolytic reprogramming in bladder cancer

doi: 10.1186/s13046-025-03591-5

Figure Lengend Snippet: Polydatin inhibits HNRNPA1 lactylation and its biological activity in bladder cancer. A Binding free energy of ten candidate compounds docked to the HNRNPA1 active pocket. B Chemical structure of polydatin. C Docking visualization of polydatin within the active pocket of HNRNPA1. D IC 50 values of polydatin in the EJ-1 cell line, as determined by CCK8 assay. E EJ-1 cells were lysed and immunoprecipitated using an anti-HNRNPA1 antibody, followed by detection of HNRNPA1-K350 lactyl lysine. F Colony formation assays were performed to assess the proliferative capacity of EJ-1 cells following 24-h treatment with 30 μM polydatin or 20 mM NaLa. G-H Tumor gross images and tumor weights were assessed in nude mice after subcutaneous injection of EJ-1 cells. Tumors were harvested on Day 19 after subcutaneous implantation. Statistical analyses were performed with unpaired two-tailed Student’s t-test ( n = 5). I Tumor volume measurements throughout the experiment. J Immunohistochemical staining visualized PKM2 levels in xenograft tumors. Scale bars: 100 μm (left panel), 50 μm (right panel). K Schematic representation of the proposed mechanism of HNRNPA1 lactylation. * p < 0.05, ** p < 0.01

Article Snippet: Cells were treated with polydatin (27208–80-6, TargetMol, USA) for 24 h to examine cell proliferation.

Techniques: Activity Assay, Binding Assay, CCK-8 Assay, Immunoprecipitation, Injection, Two Tailed Test, Immunohistochemical staining, Staining