Journal: Frontiers in Cardiovascular Medicine

Article Title: Prunetin ameliorates myocardial pyroptosis after myocardial infarction by inhibiting the TNF-α/p38 MAPK/ERK pathway

doi: 10.3389/fcvm.2026.1847407

Figure Lengend Snippet: Primer sequences.

Article Snippet: Recombinant human TNF-α protein was obtained from TargetMol (Cat. No. TMPK-00120, USA).

Techniques:

Journal: Frontiers in Cardiovascular Medicine

Article Title: Prunetin ameliorates myocardial pyroptosis after myocardial infarction by inhibiting the TNF-α/p38 MAPK/ERK pathway

doi: 10.3389/fcvm.2026.1847407

Figure Lengend Snippet: Multi-technology screening and verification of potential targets of PRU for MI therapy. (A) Chemical structure of PRU. (B) Venn diagram of PRU targets and MI-related targets. (C) PPI network. (D) Visualization of core gene PPI network. (E) GO functional enrichment analysis. (F) KEGG pathway enrichment analysis. (G) Molecular docking of PRU with targets. (H) MD simulation of PRU and TNF-α. (I) SPR assay for binding affinity between PRU and TNF-α.

Article Snippet: Recombinant human TNF-α protein was obtained from TargetMol (Cat. No. TMPK-00120, USA).

Techniques: Screening, Functional Assay, Analysis, Docking Assay, SPR Assay, Binding Assay

Journal: Frontiers in Cardiovascular Medicine

Article Title: Prunetin ameliorates myocardial pyroptosis after myocardial infarction by inhibiting the TNF-α/p38 MAPK/ERK pathway

doi: 10.3389/fcvm.2026.1847407

Figure Lengend Snippet: PRU improves cardiac function in MI mice by inhibiting TNF-α function. (A) Schematic flowchart of in vivo experiments. (B) Representative echocardiographic images from each experimental group. (C) Quantitative analysis of LVEF and LVFS, n = 5. (D,E) HE and Masson staining show representative images of cardiac tissue and quantitative analysis of cardiac fibrosis area (%), scale bar = 1,000 µm (upper), scale bar = 200 µm (lower), n = 5. Data are presented as mean ± SD from independent biological replicates. For panels (B–D) , which passed the normality assumption, one-way ANOVA followed by Tukey's post-hoc test was applied. Compared with the Sham group, ** P < 0.01, * P < 0.05; compared with the MI group, ## P < 0.01, # P < 0.05; compared with the MI + PRU group, && P < 0.01, & P < 0.05.

Article Snippet: Recombinant human TNF-α protein was obtained from TargetMol (Cat. No. TMPK-00120, USA).

Techniques: In Vivo, Analysis, Staining, Tissue, H&E Stain

Journal: Frontiers in Cardiovascular Medicine

Article Title: Prunetin ameliorates myocardial pyroptosis after myocardial infarction by inhibiting the TNF-α/p38 MAPK/ERK pathway

doi: 10.3389/fcvm.2026.1847407

Figure Lengend Snippet: Effects of PRU on TNF-α pathway proteins and oxidative stress markers in infarcted myocardium. (A) mRNA expression levels of TNF-α, IL-6, and IL-1β in cardiac tissue, n = 3. (B,C) Expression of TNF-α, p-p38, and p-ERK proteins in cardiac tissue measured and quantified by WB, n = 3. (D) Serum NT-proBNP levels in MI mice, n = 5. (E–G) Levels of SOD, MDA, and LDH in mice cardiac tissue, n = 5. Data are presented as mean ± SD from independent biological replicates. For panels (A,C,D,F,G) , which passed the normality assumption, one-way ANOVA followed by Tukey's post-hoc test was applied. For panel (E) , which violated the normality assumption, the Kruskal–Wallis test followed by Dunn's post-hoc test was used for multiple comparisons. Compared with the Sham group, ** P < 0.01, * P < 0.05; compared with the MI group, ## P < 0.01, # P < 0.05; compared with the MI + PRU group, && P < 0.01, & P < 0.05.

Article Snippet: Recombinant human TNF-α protein was obtained from TargetMol (Cat. No. TMPK-00120, USA).

Techniques: Expressing, Tissue, Real-time Polymerase Chain Reaction, Western Blot

Journal: Frontiers in Cardiovascular Medicine

Article Title: Prunetin ameliorates myocardial pyroptosis after myocardial infarction by inhibiting the TNF-α/p38 MAPK/ERK pathway

doi: 10.3389/fcvm.2026.1847407

Figure Lengend Snippet: PRU ameliorates OGD-induced injury in cardiac organoids by inhibiting TNF-α. (A) Schematic diagram of the experimental timeline for cardiac organoid treatment. (B) Viability of cardiac organoids in response to treatment with PRU and R848, n = 6. (C) Concentrations of NT-proBNP in cardiac organoid culture supernatants measured by ELISA, n = 6. (D–F) Levels of LDH, MDA and SOD in the supernatant of cardiac organoids, n = 6. (G) Representative images of cardiac organoids stained with HE and Masson, along with quantitative analysis of cardiac fibrosis area (%), scale bar = 1,000 µm, n = 3. Data are presented as mean ± SD from independent biological replicates. For panels (B,C,F,G) , which passed the normality assumption, one-way ANOVA followed by Tukey's post-hoc test was applied. For panels (D,E) , which violated the normality assumption, the Kruskal–Wallis test followed by Dunn's post-hoc test was used for multiple comparisons. Compared with the Control group, ** P < 0.01, * P < 0.05; compared with the OGD group, ## P < 0.01, # P < 0.05; compared with the OGD + PRU group, && P < 0.01, & P < 0.05.

Article Snippet: Recombinant human TNF-α protein was obtained from TargetMol (Cat. No. TMPK-00120, USA).

Techniques: Organoids, Enzyme-linked Immunosorbent Assay, Staining, Analysis, Control, H&E Stain

Journal: Frontiers in Cardiovascular Medicine

Article Title: Prunetin ameliorates myocardial pyroptosis after myocardial infarction by inhibiting the TNF-α/p38 MAPK/ERK pathway

doi: 10.3389/fcvm.2026.1847407

Figure Lengend Snippet: Mechanism underlying the protective effect of PRU against OGD-induced injury in cardiac organoids. (A,B) Expression and quantitative analysis of TNF-α, p-p38, and p-ERK in cardiac organoids, scale bar = 100 µm, n = 3. (C,D) Expression and quantitative analysis of GSDMD in cardiac organoids, scale bar = 100 µm, n = 3. (E) The levels of TNF-α and IL-1β in the supernatant of cardiac organoids were determined by ELISA, n = 6. Data are presented as mean ± SD from independent biological replicates. For panels (B,E) , which passed the normality assumption, one-way ANOVA followed by Tukey's post-hoc test was applied. For panel (D) , which violated the normality assumption, the Kruskal–Wallis test followed by Dunn's post-hoc test was used for multiple comparisons. Compared with the Control group, ** P < 0.01, * P < 0.05; compared with the OGD group, ## P < 0.01, # P < 0.05; compared with the OGD + PRU group, && P < 0.01, & P < 0.05.

Article Snippet: Recombinant human TNF-α protein was obtained from TargetMol (Cat. No. TMPK-00120, USA).

Techniques: Organoids, Expressing, Analysis, Enzyme-linked Immunosorbent Assay, Control, Immunofluorescence

Journal: iScience

Article Title: Sulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cells

doi: 10.1016/j.isci.2026.117627

Figure Lengend Snippet: SUR1 interacted with PARP1 to suppress DNA damage repair and induce apoptosis of bronchial epithelial cells (A) Co-immunoprecipitation and western blot analyses of HEK293T cells transfected with FLAG-SUR1 plasmids (left) or human bronchial epithlial (HBE) cells (right). (B) Immunofluorescence staining of HBE cells. Scale bars, 25 μm. (C) Homologous recombination reporter assay in U2OS-DRGFP cells transfected with SUR1 siRNA, followed by flow cytometry analysis. (D) Western blot analysis of HBE cells transfected with SUR1 siRNAs with or without 20 ng/mL TNF-α or 50 μg/mL LPS treatment for 1 h. (E) ROS levels in HBE cells with SUR1 knockdown, treated with or without TNF-α 20 ng/mL for 3 h. (F) Apoptosis assay by flow cytometry in HBE cells transfected with SUR1 siRNAs and treated with TNF-α. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. Co-localization in (B) was assessed using Pearson’s correlation coefficient. Data in (C–F) were analyzed using two-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.

Article Snippet: Recombinant human TNF-α protein , ABclonal Biotechnology , Cat# RP00001.

Techniques: Co-Immunoprecipitation Assay, Western Blot, Transfection, Immunofluorescence, Staining, Homologous Recombination, Reporter Assay, Flow Cytometry, Analysis, Knockdown, Apoptosis Assay

Journal: iScience

Article Title: Sulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cells

doi: 10.1016/j.isci.2026.117627

Figure Lengend Snippet: Glibenclamide disrupted SUR1-PARP1 interaction to restore DNA repair and attenuate apoptosis and inflammation in HBE cells (A) Schematic diagram of HBE cells with different treatments, followed by RNA sequencing analysis. Groups: control, 20 ng/mL; TNF-α, 100 μmol/L; glibenclamide plus TNF-α. n = 2 per group. (B) Venn diagram of differentially expressed genes. (C) GO and KEGG enrichment analyses of 280 genes in the intersection shown in (B). (D) RT-qPCR analysis of HBE cells with different treatments as indicated. (E) Co-immunoprecipitation assay in HBE cells transfected with FLAG-SUR1 plasmids and treated with 20 ng/mL TNF-α or 100 μmol/L glibenclamide as indicated. L.E., long exposure. (F) HBE cells were treated as in (E), then subjected to cytoplasmic and nuclear protein fractionation followed by western blotting. Cyto, cytoplasm; Nu, nucleus. (G) Western blot analysis of HBE cells pretreated with 100 μmol/L glibenclamide for 30 min followed by TNF-α or LPS co-treatment for 1 h. (H–J) ROS production, caspase-3 activity, and apoptosis in HBE cells under indicated treatments. (K–M) HBE cells were pretreated with 100 μmol/L glibenclamide, 5 μmol/L olaparib, or their combination for 24 h, followed by 20 ng/mL TNF-α stimulation, and subjected to western blotting, caspase-3 activity assay, and apoptosis analysis by flow cytometry. Gli, glibenclamide. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. GO and KEGG enrichment analyses in (C) were performed using a hypergeometric test with false discovery rate (FDR) correction. Data in (D) and (G–M) were analyzed using one-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.

Article Snippet: Recombinant human TNF-α protein , ABclonal Biotechnology , Cat# RP00001.

Techniques: RNA Sequencing, Analysis, Control, Quantitative RT-PCR, Co-Immunoprecipitation Assay, Transfection, Fractionation, Western Blot, Activity Assay, Caspase-3 Activity Assay, Flow Cytometry

Journal: iScience

Article Title: Sulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cells

doi: 10.1016/j.isci.2026.117627

Figure Lengend Snippet: Schematic illustration of the role of SUR1 in ALI and the protective mechanism of glibenclamide TNF-α binds to its receptor (TNFR), activating the NF-κB pathway and promoting inflammation through increased transcription of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α). In parallel, TNF-α induces mitochondrial dysfunction and ROS production, leading to DNA strand breaks. In response to DNA damage, nuclear PARP1 is activated to recruit DNA repair enzymes, promoting cell survival. Left, SUR1 interacts with and sequesters PARP1, impairing DNA damage repair. Accumulated DNA damage amplifies ROS production and NF-κB activation, which in turn further increases the transcription of inflammatory cytokines. This creates a positive feedback loop that promotes epithelial cell apoptosis and inflammation, contributing to ALI progression. Right, glibenclamide binds to SUR1 and disrupts the SUR1-PARP1 interaction, releasing PARP1 to restore DNA damage repair. This intervention breaks the pathological feedback loop by reducing ROS production, NF-κB activation, and inflammatory cytokine expression, thereby suppressing apoptosis and inflammation in epithelial cells and ultimately protecting against ALI.

Article Snippet: Recombinant human TNF-α protein , ABclonal Biotechnology , Cat# RP00001.

Techniques: Activation Assay, Expressing

Journal: iScience

Article Title: Sulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cells

doi: 10.1016/j.isci.2026.117627

Figure Lengend Snippet:

Article Snippet: Recombinant human TNF-α protein , ABclonal Biotechnology , Cat# RP00001.

Techniques: Cell-Signaling, Recombinant, Transfection, Caspase-3 Activity Assay, Protein Extraction, Knock-Out, Sequencing, Control, Plasmid Preparation, Software, Analysis