human gc ags cells  (ATCC)

Journal: International Journal of Molecular Medicine

Article Title: IL-37/IL-1R8 blocks keratinocyte acantholysis via suppressing ADAM17/EGFR

doi: 10.3892/ijmm.2026.5793

Figure Lengend Snippet: IL-37/IL-1R8 protects HaCaT cells from keratinocyte dissociation and apoptosis through the ADAM17/EGFR pathway. (A) Protein expression levels of ADAM17, p-EGFR, total EGFR as well as EGFR downstream protein p-AKT, p-ERK1/2 and p-STAT3 levels were determined by western blotting. HaCaT cells were treated with EGFR activator NSC228155. (B) Cell dissociation was analyzed by cell dissociation assay. (C) Cell apoptosis was analyzed by flow cytometry. (D) Protein expression levels of Bcl-2 and Bax were analyzed by western blotting. (E) HaCaT was transfected with ADAM17 siRNA and the transfection efficiency was detected by western blotting. HaCaT cells were transfected with ADAM17 siRNA or treated with 1 μ M of EGFR inhibitor AG1478 for 30 min followed by treated with AK23. (F) Cell dissociation was analyzed by cell dissociation assay. (G) Cell apoptosis was analyzed by flow cytometry. # P<0.05 vs. Control group; & P<0.05 vs. anti-Dsg3 group; @ P<0.05 vs. anti- Dsg3 + IL-37 + si-NC group; * P<0.05; Data are presented as mean ± SD, n=3 biological indepen- dent replicates. One-way ANOVA with Bonferroni's post-hoc test was used for multiple group comparisons. IL, interleukin; ADAM17, TNF-alpha-converting enzyme; EGFR, epidermal growth factor receptor; p- phosphorylated; STAT, signal transducer and activator of transcription; si, short interfering.

Article Snippet: For EGFR inhibition assay, HaCaT cells were pre-treated with 1 μ M of EGFR inhibitor AG1478 (MedChemExpress) at 37°C for 30 min followed by treatment with AK23 for 24 h at 37°C.

Techniques: Expressing, Western Blot, Flow Cytometry, Transfection, Control

Journal: iScience

Article Title: Ether phospholipids modulate somatosensory responses by tuning multiple receptor functions in Drosophila

doi: 10.1016/j.isci.2026.115209

Figure Lengend Snippet: Establishment of ePL-producing S2R+ cells (A) Synthesis pathway of ePLs. Two strategies to increase ePL production in Drosophila are shown. (i) Supplementation with 16-AG or 18-AG (1-alkylglycerol) or (ii) AGPS overexpression with 18-OH (fatty alcohol) supplementation. DHAP, dihydroxyacetone phosphate; MGAT, monoacylglycerol acyltransferase; CDP, cytidine diphosphate; CPT, choline phosphotransferase; and CEPT, choline/ethanolamine phosphotransferase. (B–E) Lipid composition in control and ePL-producing S2R+ cells ( n = 4) for total ePE area% of total PE (B), total ePC area% of total PC (C), and colormap for the composition of PE (D) and PC (E) species (area% of total PE or PC) in control cells (Control/S2R+), 100 μM 16-AG supplemented cells (16-AG/S2R+), dAGPS-expressing cells (Control/S2R+ dAGPS), and 100 μM 18-OH supplemented dAGPS -expressing cells (18-OH/S2R+ dAGPS). Phospholipid molecules are listed as PE (X:Y) or PC (X:Y), where X and Y denote the total number of carbon molecules in acyl chains and double bonds in acyl chains, respectively. Cross marks in (D, E) indicate phospholipid species under detectable levels. Each point represents a biological replicate. Data are presented as mean ± SEM. ∗∗∗ p < 0.01; Student’s t test. See also and and .

Article Snippet: 1- O -hexadecyl-rac-glycerol (16-AG) , Santa Cruz , sc-205917.

Techniques: Over Expression, Control, Expressing

Journal: Signal Transduction and Targeted Therapy

Article Title: Acyl-CoA-binding protein (ACBP): a poor-prognosis biomarker in sepsis and a target for disease mitigation

doi: 10.1038/s41392-026-02670-z

Figure Lengend Snippet: ACBP/DBI levels are elevated in human sepsis. a Plasma from patients with sepsis or septic shock was collected on day 1 of intensive care unit (ICU) admission. Individuals recovering from surgery in the ICU were used as controls. b Plasma human ACBP (hACBP) levels were measured by ELISA: ICU Controls ( n = 18), Sepsis patients ( n = 4), and septic shock patients ( n = 21). c hACBP levels in plasma from survivors of septic shock ( n = 12) and non-survivors ( Exitus ) ( n = 9). d Plasma hACBP levels positively correlate with lactate, a prognostic marker in sepsis. e Hierarchically clustered correlation matrix highlighting different clinical parameters positively correlating with hACBP across all patients. f Receiver-operating characteristic (ROC) curves describing the predictive performance of plasma hACBP, SAPS II, and their combination in identifying which septic patients (n = 25) died following diagnosis. g Plasma from patients was collected upon hospital admission: Controls (healthy volunteers, n = 121), and patients with Sepsis ( n = 111), Septic shock ( n = 119), or non-infectious systemic inflammatory response syndrome (SIRS, n = 73). h Plasma hACBP levels were measured by ELISA. i hACBP levels in plasma from survivors ( n = 73) and non-survivors ( n = 38) with sepsis; or j from survivors ( n = 63) and non-survivors ( n = 56) with septic shock. k Hierarchically clustered correlation matrix showing different clinical parameters positively correlating with hACBP within patients with sepsis, septic shock, or SIRS. l Receiver operating characteristic (ROC) curves showing the predictive performance of plasma hACBP, SOFA score, and their combination in identifying mortality in septic patients from a second cohort ( n = 230). m Kaplan–Meier survival curves stratified by median hACBP levels (cut-off: 80.42 ng/mL) in all septic patients ( n = 230) showing worse prognosis in the “High hACBP” group ( p = 0.012). n C57Bl/6J mice (9–12 weeks old) were injected with lipopolysaccharide (LPS, 20 mg/kg B.W. i.p.) or Escherichia coli (2.5 × 10⁶ CFU/mouse i.p.) and subjected to the cecal ligation and puncture (CLP) procedure ( n = 5–20 mice per group). Murine ACBP (mACBP) was measured in plasma from o LPS-treated mice, p E. coli -injected mice, and q CLP-subjected mice at the indicated time points. Data in ( b , c , h , i , j ) are presented as box-and-whisker plots showing the median, interquartile range, and whiskers extending from minimum to maximum values. Individual data points are overlaid. Comparisons between groups were performed using Kruskal–Wallis or Wilcoxon signed-rank tests for plasma hACBP levels. Spearman correlation coefficients and p values were used for heatmaps and individual correlations. AUC confidence intervals in ROC curves were calculated using DeLong’s method. Kaplan–Meier survival analyses were stratified by median hACBP values, and significance assessed by the log-rank test. For in vivo mouse experiments, data are displayed as means ± SEM, and two-tailed unpaired Student’s t-tests were used. SIRS systemic inflammatory response syndrome, eGFR estimated glomerular filtration rate, WB whole blood, GGT γ-glutamyltransferase, ALP alkaline phosphatase, AST aspartate transaminase, ALT alanine transaminase, CK-MB creatine kinase-MB, CK creatine kinase, cTnI cardiac troponin I, CRP C-reactive protein, SAPS II Simplified Acute Physiology Score II, MCH mean corpuscular hemoglobin, MCHC mean corpuscular hemoglobin concentration, MPV mean platelet volume, RBC red blood cells, APACHE II Acute Physiology and Chronic Health Evaluation II, SOFA Sequential Organ Failure Assessment, SOFA-CV SOFA cardiovascular subscore

Article Snippet: Eight-week-old male C57Bl/6J mice (Envigo, Gannat, France) were purchased and allowed to acclimate for 1 week.

Techniques: Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Marker, Biomarker Discovery, Injection, Ligation, Whisker Assay, In Vivo, Two Tailed Test, Filtration, Concentration Assay

Journal: Signal Transduction and Targeted Therapy

Article Title: Acyl-CoA-binding protein (ACBP): a poor-prognosis biomarker in sepsis and a target for disease mitigation

doi: 10.1038/s41392-026-02670-z

Figure Lengend Snippet: ACBP/DBI neutralization improves survival and mitigates cardiovascular dysfunction in a model of LPS-induced endotoxemia. a Twelve-week-old C57BL/6J mice were treated with either a monoclonal antibody against ACBP/DBI (α-ACBP) or an IgG2a isotype control (2.5 mg/kg body weight, i.p.), administered twice prior to LPS challenge. b Survival was monitored following LPS challenge (10 mg/kg body weight, i.p.) in mice ( n = 17–20 per group). Statistical significance was assessed using the log-rank test. c Body temperature was measured 12 h post-LPS injection. d Plasma levels of interleukin-1β (IL-1β) were quantified 6 h post-LPS injection. e Primary hepatocytes isolated from inducible whole-body Acbp/Dbi knockout ( Acbp/Dbi −/− ) and control mice were treated in vitro with LPS (250 or 1000 ng/mL), and inflammatory gene expression was assessed by RT-qPCR at 6 h post-LPS. f Plasma cardiac troponin I (cTnI) levels were measured 12 h post-LPS (20 mg/kg body weight) in mice treated with or without α-ACBP. g Representative M-mode echocardiographic tracings of the left ventricle (LV) were obtained. h Principal component analysis (PCA) of echocardiographic parameters. i Heatmap of individual echocardiographic measurements. j Twelve-week-old C57BL/6J mice were treated with either the recombinant protein ACBP/DBI (recACBP, 8 mg/kg body weight, i.v.) or PBS (i.v.), administered once prior to LPS challenge, and twice post-LPS. k Survival was monitored following LPS challenge (10 mg/kg body weight, i.p.) in mice ( n = 5–13 per group). Statistical significance was assessed using the log-rank test. All results are presented as mean ± SEM ( n = 5–10 mice per group). Group comparisons were performed using one-way ANOVA followed by pairwise comparisons. For heatmap comparisons, p values were adjusted using false discovery rate (FDR) correction. Multivariate ANOVA followed by pairwise t-tests with FDR correction was used for group comparisons in PCA (PC1–PC2). LVAW;d LV anterior wall thickness in diastole, Internal diameter;d LV internal diameter in diastole, Internal diameter;s LV internal diameter in systole, LVPW;d LV posterior wall thickness in diastole, LV Mass estimated LV muscle mass

Article Snippet: Eight-week-old male C57Bl/6J mice (Envigo, Gannat, France) were purchased and allowed to acclimate for 1 week.

Techniques: Neutralization, Control, Injection, Clinical Proteomics, Isolation, Knock-Out, In Vitro, Gene Expression, Quantitative RT-PCR, Recombinant

Journal: Signal Transduction and Targeted Therapy

Article Title: Acyl-CoA-binding protein (ACBP): a poor-prognosis biomarker in sepsis and a target for disease mitigation

doi: 10.1038/s41392-026-02670-z

Figure Lengend Snippet: ACBP/DBI blockade increases resistance to E. coli infection. a Twelve-week-old male C57BL/6J mice were treated with monoclonal antibody against ACBP/DBI (α-ACBP; 5 mg/kg, i.p.) twice during the week prior to E. coli challenge, followed by two additional doses (2.5 mg/kg, i.p.) at 4 h and 1 h before infection. b Survival was monitored in mice ( n = 10 per group) challenged intraperitoneally with 2.5 × 10⁶ CFU/mouse of E. coli . Statistical significance was assessed using the log-rank test. c Blood was collected at 1 h, 6 h, and 24 h post-infection (1 × 10⁶ CFU/mouse), plated on agar, and incubated overnight (O/N) at 37 °C for CFU counting ( n = 4–8 mice per group). At 6 h and 24 h post-infection, d PLF, e spleens, and f kidneys were collected and processed for CFU quantification. g Mice were pre-treated with α-ACBP as in ( a ) and additionally injected with clodronate liposomes (100 µL/10 g body weight, i.v.) or control liposomes 48 h before infection, and anti-mouse Ly6G (clone 1A8, 50 µg/mouse) or isotype control IgG2a 36 h and 12 h prior to E. coli injection. Two doses of α-ACBP (2.5 mg/kg) were also administered prior to infection ( n = 7–18 mice per group). At 24 h post-infection, h spleens and i kidneys were collected for CFU analysis. j Twelve-week-old male C57BL/6J mice ( n = 15 mice per group) were challenged with E. coli , and 30 min after treated with the monoclonal antibody against ACBP/DBI (α-ACBP; 10 mg/kg, i.p.). k At 36 h post-infection, spleens were collected and processed for CFU quantification. l Bone marrow-derived neutrophils (BMDNs) or bone marrow-derived macrophages (BMDMs) were isolated from male C57BL/6J mice and treated with α-ACBP (5 µg/mL) or IgG2a control for 16 h. m A bacterial killing assay was performed with BMDNs (≥80% Ly6G⁺), and E. coli (MOI = 10); CFU/mL were quantified the following day ( n = 5 mice per group). n Killing efficiency of BMDNs was calculated after 45 min of bacterial clearance. o BMDMs were differentiated over 7 days (≥70–80% F4/80⁺), then stimulated with LPS (100 ng/mL) + IFNγ (25 ng/mL) or IL-4 (25 ng/mL) + IL-13 (25 ng/mL) for 24 h, and treated with α-ACBP or IgG2a control for 16 h ( n = 6 mice per group). Killing assays were performed with E. coli (MOI = 10), and CFU/mL were determined after overnight incubation. p Bacterial killing by BMDMs was quantified after 120 min and expressed as absolute values of [CFU/mL/min]. q BMDMs from male C57BL/6J and Gabrg2 F77I/F77I mice were differentiated over 7 days (≥70–80% F4/80⁺), then stimulated with LPS (100 ng/mL) + IFNγ (25 ng/mL) or IL-4 (25 ng/mL) + IL-13 (25 ng/mL) for 24 h ( n = 6 mice per group). Killing assays were performed with E. coli (MOI = 10), and bacterial killing by BMDMs was quantified after 120 min and expressed as absolute values of CFU/mL/min. Data are presented as means ± SEM. Statistical comparisons were performed using one-way or two-way ANOVA with estimation of marginal means for pairwise comparisons, or Student’s t-test where applicable. l was generated with “BioRender.com.” IFNγ interferon-γ, IL-4 interleukin-4, IL-13 interleukin-13, MOI multiplicity of infection, CFU colony-forming units, PLF peritoneal lavage fluid

Article Snippet: Eight-week-old male C57Bl/6J mice (Envigo, Gannat, France) were purchased and allowed to acclimate for 1 week.

Techniques: Infection, Incubation, Injection, Liposomes, Control, Derivative Assay, Isolation, Generated

Journal: Signal Transduction and Targeted Therapy

Article Title: Acyl-CoA-binding protein (ACBP): a poor-prognosis biomarker in sepsis and a target for disease mitigation

doi: 10.1038/s41392-026-02670-z

Figure Lengend Snippet: Neutralization of ACBP/DBI reduces sepsis-associated damage induced by CLP in mice. a Nine-week-old male C57BL/6J mice were treated with monoclonal antibody against ACBP/DBI (α-ACBP; 2.5 mg/kg, i.p.) or isotype control, followed 4 h later by high-grade CLP surgery. Additional doses of α-ACBP (5 mg/kg, i.p.) or IgG isotype were administered 90 min before sample collection at 24 h. b Survival was monitored in CLP-treated groups ( n = 9–10 per group). The p value from the log-rank test is shown. c Body temperature was recorded at 24 h post-CLP. Plasma markers of organ injury and inflammation were measured at 24 h: d blood urea nitrogen (BUN), e alanine aminotransferase (ALT), f aspartate transaminase (AST), and g mACBP/DBI. h Plasma levels of 43 cytokines were measured at 24 h post-CLP using a proximity extension assay. Cytokine expression was compared among control mice (Sham) or those submitted to CLP and treated with α-ACBP or isotype. Statistical comparisons were performed by two-way ANOVA with FDR correction for multiple comparisons on log2-normalized cytokine data. i Immune cell populations in the kidney were analyzed by flow cytometry 24 h post-CLP ( n = 5–12 mice per group). Fourteen populations were defined within CD45⁺CD11b⁺ cells using manual gating, and median fluorescence intensity (MFI) of each marker is represented in a heatmap. j Relative abundance of selected kidney immune clusters that were significantly modulated by ACBP neutralization is shown as a percentage of CD45⁺CD11b⁺ cells, comparing septic and control mice. k Similarly, 13 immune populations were defined in the heart within CD45⁺CD11b⁺ cells, with the corresponding MFI heatmap shown ( n = 5–12 mice per group). l Relative abundance of significant heart immune populations affected by ACBP neutralization is displayed as a percentage of CD45⁺CD11b⁺ cells. Data are presented as means ± SEM. Statistical comparisons were performed using one-way ANOVA with estimation of marginal means for pairwise comparisons. Immune population analyses used two-way ANOVA followed by pairwise comparisons. Compensation, scaling, and gating strategies were conducted using the Omiq.ai platform

Article Snippet: Eight-week-old male C57Bl/6J mice (Envigo, Gannat, France) were purchased and allowed to acclimate for 1 week.

Techniques: Neutralization, Control, Clinical Proteomics, Expressing, Flow Cytometry, Fluorescence, Marker

Journal: Signal Transduction and Targeted Therapy

Article Title: Acyl-CoA-binding protein (ACBP): a poor-prognosis biomarker in sepsis and a target for disease mitigation

doi: 10.1038/s41392-026-02670-z

Figure Lengend Snippet: Genetic ablation or therapeutic neutralization of ACBP/DBI protects against CLP-induced damage and senescence. Bacterial clearance was improved by ACBP/DBI neutralization in a peritoneal fluid lavage (PFL) at 6 h post-CLP, and in b spleen, c kidney, and d liver 24 h post-CLP ( n = 5–10 mice per group). e Representative immunohistochemistry (IHC) images showing p21 senescence marker in livers of Sham controls or CLP mice treated with α-ACBP, and quantification of p21⁺ IHC signal indicating increased p21 presence in CLP livers, which is reduced by α-ACBP treatment ( n = 4–6 mice per group). f Nine-week-old male C57BL/6J mice were treated with α-ACBP (2.5 mg/kg, i.p.) twice in combination with one dose of diazepam (DZP, 4 mg/kg, i.p.) 4 h prior to sham or CLP surgery. g Survival was monitored over time ( n = 5–10 per group). The p value of the log-rank test is indicated. h Nine-week-old inducible whole-body Acbp/Dbi knockout (Acbp/Dbi −/− ) or control male mice were injected with tamoxifen for 5 consecutive days prior to sham or CLP surgery. i Survival was monitored post-surgery ( n = 7–14 per group). Statistical significance was determined using the log-rank test. j Body temperature was measured at 24 h following CLP. Plasma levels of k ALT, l AST, and m BUN were assessed ( n = 5–18 mice per group). n Nine-week-old male C57BL/6J mice were treated with monoclonal antibody against ACBP/DBI (α-ACBP; 10 mg/kg, i.p.) or isotype control, 6 h after high-grade CLP surgery and every 48 h. o Survival was monitored in CLP-treated groups ( n = 20 per group). The p value from the log-rank test is shown. p Body temperature was recorded at 24 h post-CLP. Data are presented as means ± SEM. Statistical comparisons were performed using one-way ANOVA with estimation of marginal means for pairwise comparisons, or Student’s t-test, where applicable

Article Snippet: Eight-week-old male C57Bl/6J mice (Envigo, Gannat, France) were purchased and allowed to acclimate for 1 week.

Techniques: Neutralization, Immunohistochemistry, Marker, Knock-Out, Control, Injection, Clinical Proteomics

Journal: Signal Transduction and Targeted Therapy

Article Title: Acyl-CoA-binding protein (ACBP): a poor-prognosis biomarker in sepsis and a target for disease mitigation

doi: 10.1038/s41392-026-02670-z

Figure Lengend Snippet: Neutralization of ACBP/DBI combined with dexamethasone enhances protection against LPS-induced challenge and CLP-induced sepsis in mice. a Twelve-week-old male C57BL/6J mice were treated with monoclonal antibody against ACBP/DBI (α-ACBP; 5 mg/kg, i.p.) twice, in combination with one dose of dexamethasone (DEX; 10 mg/kg, i.p.) during the week prior to LPS challenge. Additionally, two doses of α-ACBP (2.5 mg/kg) and one dose of DEX (10 mg/kg) were administered 4 h or 1 h before LPS injection. b Survival was monitored in LPS-challenged mice ( n = 20 per group). The p value from the log-rank test is shown. c Plasma levels of 42 cytokines were measured at 6 h post-LPS challenge using a proximity extension assay. Cytokine expression was compared among groups treated with α-ACBP, DEX, both, or vehicle. Statistical comparisons were performed by two-way ANOVA with FDR correction for multiple comparisons on log2-normalized cytokine data. d Nine-week-old male C57BL/6J mice were treated with α-ACBP (2.5 mg/kg, i.p.) twice in combination with one dose of DEX (10 mg/kg, i.p.) 1 h prior to sham or CLP surgery. e Survival was monitored over time (n = 15–20 per group). The p value of the log-rank test is indicated. f Body temperature was recorded 24 h post-surgery. g Murine Sepsis Score (MSS) was assessed on a scale of 0 to 4 based on multiple clinical parameters—appearance (App), respiration quality (RQ), respiration rate (RR), eyes, level of consciousness (LOC), activity, and response to stimulus (RTS)—by two independent examiners. Scores were averaged per mouse and depicted as Z-scores in a heatmap analyzed by two-way ANOVA with FDR correction. h Individual MSS values are shown. i Venn diagram illustrating overlap among upregulated differentially expressed genes (DEGs) in spleens from CLP mice, categorizing genes reversed by α-ACBP alone, by DEX alone, or specifically by the combination treatment. j Venn diagram showing overlap of downregulated DEGs in the same groups. Data are presented as means ± SEM. Statistical comparisons were performed using one-way ANOVA ( h ) and two-way ANOVA ( f ) with estimation of marginal means for pairwise comparisons. il1b interleukin-1 beta, ifnl2 interferon lambda 2, il9 interleukin-9, il17f interleukin-17f, ifng interferon gamma, il17a interleukin-17a, ccl17 c-c motif chemokine ligand 17, cxcl1 c-x-c motif chemokine ligand 1, csf3 colony stimulating factor 3, il16 interleukin-16, ccl2 c-c motif chemokine ligand 2, il21 interleukin-21, cxcl12 c-x-c motif chemokine ligand 12, il7 interleukin-7, cxcl11 c-x-c motif chemokine ligand 11, il31 interleukin-31, il2 interleukin-2, il33 interleukin-33, csf1 colony stimulating factor 1, cxcl9 c-x-c motif chemokine ligand 9, ccl4 c-c motif chemokine ligand 4, hgf hepatocyte growth factor, il10 interleukin-10, il1a interleukin-1 alpha, ccl11 c-c motif chemokine ligand 11, csf2 colony stimulating factor 2, il-4 interleukin-4, ctla4 cytotoxic t-lymphocyte associated protein 4, ccl22 c-c motif chemokine ligand 22, il3 interleukin-3, cd274 cluster of differentiation 274 (pd-l1), pdcd1lg2 programmed cell death 1 ligand 2 (pd-l2), cxcl2 c-x-c motif chemokine ligand 2, ccl5 c-c motif chemokine ligand 5, fgf21 fibroblast growth factor 21, il5 interleukin-5, tnf tumor necrosis factor, il12a_il12b interleukin-12 subunits (p35 and p40), il-6 interleukin-6, il22 interleukin-22, il27 interleukin-27, ifna2 interferon alpha 2

Article Snippet: Eight-week-old male C57Bl/6J mice (Envigo, Gannat, France) were purchased and allowed to acclimate for 1 week.

Techniques: Neutralization, Injection, Clinical Proteomics, Expressing, Activity Assay

Journal: Signal Transduction and Targeted Therapy

Article Title: Acyl-CoA-binding protein (ACBP): a poor-prognosis biomarker in sepsis and a target for disease mitigation

doi: 10.1038/s41392-026-02670-z

Figure Lengend Snippet: Co-administration of DEX and ACBP/DBI neutralization ameliorates sepsis-associated cardiomyopathy following CLP surgery. a Nine-week-old male C57BL/6J mice were treated with the monoclonal antibody against ACBP/DBI (α-ACBP; 2.5 mg/kg, i.p.) twice, in combination with one dose of DEX (10 mg/kg, i.p.) administered 1 h before sham or CLP surgery. b Mean arterial pressure (MAP) was measured 24 h post-surgery in sham and CLP mice treated with α-ACBP, DEX, or both. Data are presented as means ± SEM. Statistical comparisons were performed by two-way ANOVA followed by pairwise comparisons. c Representative echocardiographic M-mode images of LV function from the treatment groups. d Quantitative analysis of LV echocardiographic parameters. Group comparisons were assessed using one-way ANOVA followed by FDR correction for multiple comparisons. Adjusted p values are reported ( n = 10–20 mice per group). e Heatmap clustered by Euclidean distance showing Z-score–normalized changes in cardiac metabolite concentrations in sham and CLP mice treated with α-ACBP, DEX, or the combination. Venn diagram showing overlap of f upregulated or g downregulated differentially expressed metabolites in CLP hearts and those reversed by α-ACBP, DEX, or their combination

Article Snippet: Eight-week-old male C57Bl/6J mice (Envigo, Gannat, France) were purchased and allowed to acclimate for 1 week.

Techniques: Neutralization