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saha  (MedChemExpress)


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    MedChemExpress saha
    HDAC2 deficiency or inhibition compromises the antimicrobial efficacy, but improves anti-inflammatory responses in the mice with sepsis. (A-D) Effects of the HDAC2-knockout or inhibition on the survival of mice <t>with</t> <t>CLP-induced</t> or LPS-induced sepsis. Kaplan-Meier curves for the HDAC2-knockout or inhibition by <t>SAHA-treated</t> mice with or CLP-induced or LPS-induced sepsis (n = 20 mice). (E-H) Serum IL-6 and IL-1β levels were determined in the sham or CLP-induced or LPS-induced septic mice treated with or without SAHA (25 mg/kg). These inflammatory parameters were measured by ELISA. Data are shown as mean ± SEM. *p < 0.05; n = 5 mice per group. (I and J) Serum AST, ALT, Urea and Crea levels were measured in sham or CLP-induced or LPS-induced septic mice treated with or without SAHA. Blood was collected by orbital sampling, and these biochemical parameters were measured by the Automatic Biochemistry Analyzer. Data are shown as mean ± SEM. **p < 0.01; n = 5 mice per group.
    Saha, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 169 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/saha/Vorinostat/pmc13131401-68-16-19
    Average 96 stars, based on 169 article reviews
    saha - by Bioz Stars, 2026-10
    96/100 stars

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    1) Product Images from "HDAC2 enhances the antimicrobial activity of neutrophils by promoting the formation of neutrophil extracellular traps (NETs) in sepsis"

    Article Title: HDAC2 enhances the antimicrobial activity of neutrophils by promoting the formation of neutrophil extracellular traps (NETs) in sepsis

    Journal: Journal of Advanced Research

    doi: 10.1016/j.jare.2025.08.041

    HDAC2 deficiency or inhibition compromises the antimicrobial efficacy, but improves anti-inflammatory responses in the mice with sepsis. (A-D) Effects of the HDAC2-knockout or inhibition on the survival of mice with CLP-induced or LPS-induced sepsis. Kaplan-Meier curves for the HDAC2-knockout or inhibition by SAHA-treated mice with or CLP-induced or LPS-induced sepsis (n = 20 mice). (E-H) Serum IL-6 and IL-1β levels were determined in the sham or CLP-induced or LPS-induced septic mice treated with or without SAHA (25 mg/kg). These inflammatory parameters were measured by ELISA. Data are shown as mean ± SEM. *p < 0.05; n = 5 mice per group. (I and J) Serum AST, ALT, Urea and Crea levels were measured in sham or CLP-induced or LPS-induced septic mice treated with or without SAHA. Blood was collected by orbital sampling, and these biochemical parameters were measured by the Automatic Biochemistry Analyzer. Data are shown as mean ± SEM. **p < 0.01; n = 5 mice per group.
    Figure Legend Snippet: HDAC2 deficiency or inhibition compromises the antimicrobial efficacy, but improves anti-inflammatory responses in the mice with sepsis. (A-D) Effects of the HDAC2-knockout or inhibition on the survival of mice with CLP-induced or LPS-induced sepsis. Kaplan-Meier curves for the HDAC2-knockout or inhibition by SAHA-treated mice with or CLP-induced or LPS-induced sepsis (n = 20 mice). (E-H) Serum IL-6 and IL-1β levels were determined in the sham or CLP-induced or LPS-induced septic mice treated with or without SAHA (25 mg/kg). These inflammatory parameters were measured by ELISA. Data are shown as mean ± SEM. *p < 0.05; n = 5 mice per group. (I and J) Serum AST, ALT, Urea and Crea levels were measured in sham or CLP-induced or LPS-induced septic mice treated with or without SAHA. Blood was collected by orbital sampling, and these biochemical parameters were measured by the Automatic Biochemistry Analyzer. Data are shown as mean ± SEM. **p < 0.01; n = 5 mice per group.

    Techniques Used: Inhibition, Knock-Out, Enzyme-linked Immunosorbent Assay, Sampling

    HDAC2 is required for NET formation. (A and B) Phagocytic uptake and intracellular killing in neutrophils were detected by flow-based assay and colon-formation assay. (A) Phagocytic uptake in neutrophils was detected by flow-based assay. Neutrophils were isolated from peripheral blood of HDAC2 KO or HDAC2 WT mice, and they were co-incubated with E. coli -GFP for two hours. (B) Intracellular killing in neutrophils was detected by colon-formation assay. Blood was taken from the tail vein of the mice, then applied to the pretreated solid MHA medium and incubated at 37 °C for 24 h. The number of bacterial clones was calculated. n = 5 mice per group. (C-D) NETs were detected in the neutrophils from peripheral blood of HDAC2 KO or HDAC2 WT mice by immunofluorescence. Representative data showing MPO-positive cells defined as positive NETs. Data are presented as the means ± SEM. of independent experiments. *P < 0.05, **P < 0.01 (two-tailed Student’s t -test). (E) NETs were detected in the neutrophils from peripheral blood of HDAC2 KO or HDAC2 WT mice by a flow cytometry-based assay. Representative flow data showing positive cells in global Histone H3 citrullination of H3R2, H3R8 or H3R17 sites, defined as positive NETs. (F) NETs markers were detected by western blotting in the neutrophils from HDAC2 WT mice after stimulation with LPS (50 μg/ml) and SAHA (5 μM). Representative data showing H3-Cit expression defined as NETs. The H3 protein was used for western blot loading controls.
    Figure Legend Snippet: HDAC2 is required for NET formation. (A and B) Phagocytic uptake and intracellular killing in neutrophils were detected by flow-based assay and colon-formation assay. (A) Phagocytic uptake in neutrophils was detected by flow-based assay. Neutrophils were isolated from peripheral blood of HDAC2 KO or HDAC2 WT mice, and they were co-incubated with E. coli -GFP for two hours. (B) Intracellular killing in neutrophils was detected by colon-formation assay. Blood was taken from the tail vein of the mice, then applied to the pretreated solid MHA medium and incubated at 37 °C for 24 h. The number of bacterial clones was calculated. n = 5 mice per group. (C-D) NETs were detected in the neutrophils from peripheral blood of HDAC2 KO or HDAC2 WT mice by immunofluorescence. Representative data showing MPO-positive cells defined as positive NETs. Data are presented as the means ± SEM. of independent experiments. *P < 0.05, **P < 0.01 (two-tailed Student’s t -test). (E) NETs were detected in the neutrophils from peripheral blood of HDAC2 KO or HDAC2 WT mice by a flow cytometry-based assay. Representative flow data showing positive cells in global Histone H3 citrullination of H3R2, H3R8 or H3R17 sites, defined as positive NETs. (F) NETs markers were detected by western blotting in the neutrophils from HDAC2 WT mice after stimulation with LPS (50 μg/ml) and SAHA (5 μM). Representative data showing H3-Cit expression defined as NETs. The H3 protein was used for western blot loading controls.

    Techniques Used: Tube Formation Assay, Isolation, Incubation, Clone Assay, Immunofluorescence, Two Tailed Test, Flow Cytometry, Western Blot, Expressing

    HDAC2 promotes NETs formation through the acetylation-citrullination pathway. (A–C) Representative images for LPS (50 μg/ml)-stimulated primary neutrophils from HDAC2 WT and HDAC2 KO mice. (A) Immunostaining for histone H3K18 acetylation (green) was performed with DNA counterstained with Hoechst 33342 (blue) and corresponding MFI of quantitative data (E). Scale bars, 20 μm. (B) Immunostaining for histone H3R17 methylation (green) was performed with DNA counterstained with Hoechst 33342 (blue) and corresponding MFI of quantitative data (F). Scale bars, 20 μm. (C) Immunostaining for histone H3R17 citrullination (green) was performed with DNA counterstained with Hoechst 33342 (blue) and corresponding MFI of quantitative data (G). Scale bars, 20 μm. (D) Histone H3R17 citrullination was regulated by H3R17 methylation inhibitor (EZM2302) and HDAC2 inhibitor (SAHA), and immunostaining for histone H3R17 citrullination (green) was performed with DNA counterstained with Hoechst 33342 (blue), the corresponding MFI of quantitative data (H). Scale bars, 20 μm. (I) H3K18 acetylation, H3R17 methylation and H3R17 citrullination were detected by western blotting in the neutrophils from HDAC2 WT and HDAC2 KO mice after stimulation with LPS (50 μg/ml). The H3 protein was used for western blot loading controls. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
    Figure Legend Snippet: HDAC2 promotes NETs formation through the acetylation-citrullination pathway. (A–C) Representative images for LPS (50 μg/ml)-stimulated primary neutrophils from HDAC2 WT and HDAC2 KO mice. (A) Immunostaining for histone H3K18 acetylation (green) was performed with DNA counterstained with Hoechst 33342 (blue) and corresponding MFI of quantitative data (E). Scale bars, 20 μm. (B) Immunostaining for histone H3R17 methylation (green) was performed with DNA counterstained with Hoechst 33342 (blue) and corresponding MFI of quantitative data (F). Scale bars, 20 μm. (C) Immunostaining for histone H3R17 citrullination (green) was performed with DNA counterstained with Hoechst 33342 (blue) and corresponding MFI of quantitative data (G). Scale bars, 20 μm. (D) Histone H3R17 citrullination was regulated by H3R17 methylation inhibitor (EZM2302) and HDAC2 inhibitor (SAHA), and immunostaining for histone H3R17 citrullination (green) was performed with DNA counterstained with Hoechst 33342 (blue), the corresponding MFI of quantitative data (H). Scale bars, 20 μm. (I) H3K18 acetylation, H3R17 methylation and H3R17 citrullination were detected by western blotting in the neutrophils from HDAC2 WT and HDAC2 KO mice after stimulation with LPS (50 μg/ml). The H3 protein was used for western blot loading controls. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Techniques Used: Immunostaining, Methylation, Western Blot

    Protective effects of HDAC2 inhibition and histone methylation inhibition in CLP-induced septic mice (A) Kaplan-Meier curves of CLP-induced septic mice treated with or without SAHA and EZM2302 (n = 20 mice). (B and C) Serum MPO, IL-6 and IL-1β levels were measured with mouse ELISA kit in the CLP-induced septic mice treated with or without SAHA and EZM2302. (D) Serum AST, ALT, Urea and Crea levels were measured in the CLP-induced septic mice treated with or without SAHA and EZM2302. Blood was collected by orbital sampling, and serum biochemical parameters were measured by the Automatic Biochemistry Analyzer. The experiments were performed in quintuplicate, data are presented as the means ± SEM. of independent experiments. *P < 0.05, **P < 0.01 (two-tailed Student’s t -test). (n = 5 mice). (E and F) Histology of lungs, kidneys and livers from mice treated with or without SAHA and EZM2302. (E) The Histology with H&E staining for lungs, kidneys and livers. (F) Cell apoptosis in lungs, kidneys and livers was stained with cleaved-caspase 3. The mice were treated with EZM2302 (25 mg/kg) two hours prior to cecal ligation and puncture (CLP), and SAHA was administered after CLP surgery. SAHA, a HDAC2 inhibitor; EZM2302, a methylation inhibitor.
    Figure Legend Snippet: Protective effects of HDAC2 inhibition and histone methylation inhibition in CLP-induced septic mice (A) Kaplan-Meier curves of CLP-induced septic mice treated with or without SAHA and EZM2302 (n = 20 mice). (B and C) Serum MPO, IL-6 and IL-1β levels were measured with mouse ELISA kit in the CLP-induced septic mice treated with or without SAHA and EZM2302. (D) Serum AST, ALT, Urea and Crea levels were measured in the CLP-induced septic mice treated with or without SAHA and EZM2302. Blood was collected by orbital sampling, and serum biochemical parameters were measured by the Automatic Biochemistry Analyzer. The experiments were performed in quintuplicate, data are presented as the means ± SEM. of independent experiments. *P < 0.05, **P < 0.01 (two-tailed Student’s t -test). (n = 5 mice). (E and F) Histology of lungs, kidneys and livers from mice treated with or without SAHA and EZM2302. (E) The Histology with H&E staining for lungs, kidneys and livers. (F) Cell apoptosis in lungs, kidneys and livers was stained with cleaved-caspase 3. The mice were treated with EZM2302 (25 mg/kg) two hours prior to cecal ligation and puncture (CLP), and SAHA was administered after CLP surgery. SAHA, a HDAC2 inhibitor; EZM2302, a methylation inhibitor.

    Techniques Used: Inhibition, Methylation, Enzyme-linked Immunosorbent Assay, Sampling, Two Tailed Test, Staining, Ligation

    Related Articles

    Ligation:

    Article Title: HDAC2 enhances the antimicrobial activity of neutrophils by promoting the formation of neutrophil extracellular traps (NETs) in sepsis
    Article Snippet: After washing with PBS, the samples were analyzed by flow cytometer (ACEA NovoCyte D2060R, China). .. The mice were treated with EZM2302 (25 mg/kg; TargetMOI, T5605, China) two hours prior to cecal ligation and puncture (CLP), and SAHA (25 mg/kg; MCE, HY-10221) was administered after CLP surgery. ..

    Concentration Assay:

    Article Title: Thymosin α1-induced secretion of the IL-15/RA complex by THP-1-derived dendritic cells restrains HIV latency in vitro .
    Article Snippet: .. The final concentration of 1μM SAHA (MCE, #HY-10221) and 10ng/mL IL-2 (Invetrogen, #PHC0026) were added to both Tα1-treated experimental group and blank control group for 48h. ..

    Control:

    Article Title: Thymosin α1-induced secretion of the IL-15/RA complex by THP-1-derived dendritic cells restrains HIV latency in vitro .
    Article Snippet: .. The final concentration of 1μM SAHA (MCE, #HY-10221) and 10ng/mL IL-2 (Invetrogen, #PHC0026) were added to both Tα1-treated experimental group and blank control group for 48h. ..

    Article Title: Thymosin α1-induced secretion of the IL-15/RA complex by THP-1-derived dendritic cells restrains HIV latency in vitro
    Article Snippet: .. The final concentrations of 1 μM SAHA (MCE, #HY-10221) and 10 ng/mL IL-2 (Invitrogen, #PHC0026) were added to both Tα1-treated experimental group and blank control group for 48 h. IL-2 sustained T-cell activity, and SAHA synergized with IL-15 to effectively reactivate HIV-1 reservoir in vitro [ , ]. .. To ascertain the pivotal role of CD8+ T cells or IL-15 in suppressing the reservoir, additional experimental groups utilized the same co-culture model with CD8+ T cell-depleted PBMCs or IL-15 antibody (R&D, # IC2471P) at a final concentration of 10 ng/mL added to the upper layer.

    other:

    Article Title: HDACi-Loaded Nanoliposomes Enhance the Diversity of Antibody CDRs in Rabbits and the Application in Antibody Preparation
    Article Snippet: SAHA, C6 was purchased from MedChemExpress (MCE, USA).

    Article Title: HDACi-Loaded Nanoliposomes Enhance the Diversity of Antibody CDRs in Rabbits and the Application in Antibody Preparation
    Article Snippet: SAHA, C6 was purchased from MedChemExpress (MCE, USA).

    CCK-8 Assay:

    Article Title: Reprogramming the epigenetic profile improves the B regulatory cell function of patients with recurrent pregnancy loss
    Article Snippet: .. SAHA (MCE, HY-10223): Tested at 0.5–5 μM (24–72 h) after validating non-toxicity via CCK-8 assay (Supplementary Fig. S1). ..

    Activity Assay:

    Article Title: Thymosin α1-induced secretion of the IL-15/RA complex by THP-1-derived dendritic cells restrains HIV latency in vitro
    Article Snippet: .. The final concentrations of 1 μM SAHA (MCE, #HY-10221) and 10 ng/mL IL-2 (Invitrogen, #PHC0026) were added to both Tα1-treated experimental group and blank control group for 48 h. IL-2 sustained T-cell activity, and SAHA synergized with IL-15 to effectively reactivate HIV-1 reservoir in vitro [ , ]. .. To ascertain the pivotal role of CD8+ T cells or IL-15 in suppressing the reservoir, additional experimental groups utilized the same co-culture model with CD8+ T cell-depleted PBMCs or IL-15 antibody (R&D, # IC2471P) at a final concentration of 10 ng/mL added to the upper layer.

    In Vitro:

    Article Title: Thymosin α1-induced secretion of the IL-15/RA complex by THP-1-derived dendritic cells restrains HIV latency in vitro
    Article Snippet: .. The final concentrations of 1 μM SAHA (MCE, #HY-10221) and 10 ng/mL IL-2 (Invitrogen, #PHC0026) were added to both Tα1-treated experimental group and blank control group for 48 h. IL-2 sustained T-cell activity, and SAHA synergized with IL-15 to effectively reactivate HIV-1 reservoir in vitro [ , ]. .. To ascertain the pivotal role of CD8+ T cells or IL-15 in suppressing the reservoir, additional experimental groups utilized the same co-culture model with CD8+ T cell-depleted PBMCs or IL-15 antibody (R&D, # IC2471P) at a final concentration of 10 ng/mL added to the upper layer.

    Inhibition:

    Article Title: HDAC2 enhances the antimicrobial activity of neutrophils by promoting the formation of neutrophil extracellular traps (NETs) in sepsis
    Article Snippet: .. For mouse models of CLP-induced sepsis with HDAC2 inhibition, the animals received an intraperitoneal injection of SAHA (25 mg/kg; MCE, HY-10221) after 0.5 h CLP modeling; For mouse models of LPS-induced sepsis with HDAC2 inhibition, the mice were injected intraperitoneally with LPS (10 mg/kg; Sigma, L4130, derived from E. coli O111:B4) after 1 h injection of SAHA. ..

    Injection:

    Article Title: HDAC2 enhances the antimicrobial activity of neutrophils by promoting the formation of neutrophil extracellular traps (NETs) in sepsis
    Article Snippet: .. For mouse models of CLP-induced sepsis with HDAC2 inhibition, the animals received an intraperitoneal injection of SAHA (25 mg/kg; MCE, HY-10221) after 0.5 h CLP modeling; For mouse models of LPS-induced sepsis with HDAC2 inhibition, the mice were injected intraperitoneally with LPS (10 mg/kg; Sigma, L4130, derived from E. coli O111:B4) after 1 h injection of SAHA. ..

    Derivative Assay:

    Article Title: HDAC2 enhances the antimicrobial activity of neutrophils by promoting the formation of neutrophil extracellular traps (NETs) in sepsis
    Article Snippet: .. For mouse models of CLP-induced sepsis with HDAC2 inhibition, the animals received an intraperitoneal injection of SAHA (25 mg/kg; MCE, HY-10221) after 0.5 h CLP modeling; For mouse models of LPS-induced sepsis with HDAC2 inhibition, the mice were injected intraperitoneally with LPS (10 mg/kg; Sigma, L4130, derived from E. coli O111:B4) after 1 h injection of SAHA. ..



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    Image Search Results


    SAHA treatment partially rescues histone hypoacetylation and restores memory performance in NOR (A) Outline of the experimental design. (B) Purified histone proteins from hippocampi immunoblotted for AcH3K9/K14 and total H4 in WT and TS with and without treatment with SAHA (top) and densitometric ratios of AcH3K9/K14 normalized to total H4 (bottom). N = 4/5 per group. Data are depicted as means ± SEM, with individual mice represented by points. Kruskal-Wallis test followed by pairwise Wilcoxon tests with multiple-comparison correction ∗ p < 0.05. (C) NOR performance before (left) and after (right) SAHA treatment. WT N = 21 males and 19 females, TS N = 14 males and 16 females, TS + SAHA N = 9 males and 21 females. Data are represented as boxplots. Two-way ANOVA; Tukey’s HSD as post hoc; ∗∗∗ p < 0.001. See also .

    Journal: iScience

    Article Title: HDAC inhibitor treatment restores transcriptome, chromatin accessibility, and memory deficits in a mouse model for Down syndrome

    doi: 10.1016/j.isci.2026.117670

    Figure Lengend Snippet: SAHA treatment partially rescues histone hypoacetylation and restores memory performance in NOR (A) Outline of the experimental design. (B) Purified histone proteins from hippocampi immunoblotted for AcH3K9/K14 and total H4 in WT and TS with and without treatment with SAHA (top) and densitometric ratios of AcH3K9/K14 normalized to total H4 (bottom). N = 4/5 per group. Data are depicted as means ± SEM, with individual mice represented by points. Kruskal-Wallis test followed by pairwise Wilcoxon tests with multiple-comparison correction ∗ p < 0.05. (C) NOR performance before (left) and after (right) SAHA treatment. WT N = 21 males and 19 females, TS N = 14 males and 16 females, TS + SAHA N = 9 males and 21 females. Data are represented as boxplots. Two-way ANOVA; Tukey’s HSD as post hoc; ∗∗∗ p < 0.001. See also .

    Article Snippet: Vorinostat (SAHA) , Selleck Chemicals LLC , Cat#S1047.

    Techniques: Purification, Comparison

    SAHA rescues chromatin and transcriptomic changes (A) Outline of the experimental strategy. (B) PCA plot of ATAC-seq data obtained from four WT, five TS mice, and three TS-SAHA (TST). (C) PCA plot of RNA-seq data obtained from four WT and four TS mice and three TS-SAHA (TST). (D) Number of differentially accessible regions (DARs) for each comparison (left), and number of DARs in non-triplicated and triplicated genomic regions (right). (E) Number of differentially expressed genes (DEGs) for each comparison (left) and number of DEGs in non-triplicated and triplicated genomic regions (right). (F) Analysis of differentially accessible regions (DARs) in TS neurons and their rescue upon SAHA treatment, shown as line-plots (left) and Venn diagram (left). Kruskal-Wallis test followed by pairwise Wilcoxon tests with multiple-comparison correction, ∗∗∗ p < 0.001. (G) Analysis of differentially expressed genes (DEGs) in TS neurons and their rescue upon SAHA treatment, shown as line-plots (left) and Venn diagram (right). Kruskal-Wallis test followed by pairwise Wilcoxon tests with multiple-comparison correction, ∗∗∗ p < 0.001. (H) Heatmap of transcription factor motif enrichment among gained peaks in TS and TS-SAHA neurons, with significance and fold enrichment. (I) Gene set enrichment analysis of differentially expressed genes in TS (red) and TS-SAHA neurons (orange). See also .

    Journal: iScience

    Article Title: HDAC inhibitor treatment restores transcriptome, chromatin accessibility, and memory deficits in a mouse model for Down syndrome

    doi: 10.1016/j.isci.2026.117670

    Figure Lengend Snippet: SAHA rescues chromatin and transcriptomic changes (A) Outline of the experimental strategy. (B) PCA plot of ATAC-seq data obtained from four WT, five TS mice, and three TS-SAHA (TST). (C) PCA plot of RNA-seq data obtained from four WT and four TS mice and three TS-SAHA (TST). (D) Number of differentially accessible regions (DARs) for each comparison (left), and number of DARs in non-triplicated and triplicated genomic regions (right). (E) Number of differentially expressed genes (DEGs) for each comparison (left) and number of DEGs in non-triplicated and triplicated genomic regions (right). (F) Analysis of differentially accessible regions (DARs) in TS neurons and their rescue upon SAHA treatment, shown as line-plots (left) and Venn diagram (left). Kruskal-Wallis test followed by pairwise Wilcoxon tests with multiple-comparison correction, ∗∗∗ p < 0.001. (G) Analysis of differentially expressed genes (DEGs) in TS neurons and their rescue upon SAHA treatment, shown as line-plots (left) and Venn diagram (right). Kruskal-Wallis test followed by pairwise Wilcoxon tests with multiple-comparison correction, ∗∗∗ p < 0.001. (H) Heatmap of transcription factor motif enrichment among gained peaks in TS and TS-SAHA neurons, with significance and fold enrichment. (I) Gene set enrichment analysis of differentially expressed genes in TS (red) and TS-SAHA neurons (orange). See also .

    Article Snippet: Vorinostat (SAHA) , Selleck Chemicals LLC , Cat#S1047.

    Techniques: RNA Sequencing, Comparison, Analysis

    SAHA transcriptional rescue is mediated by heterochromatization of the triplicated region (A) Venn diagram showing the fraction of triplicated genes whose expression is rescued by SAHA treatment. One-sided Fisher’s exact test. (B) Correlation between the overexpression of triplicated genes and of normalization after SAHA treatment (Pearson’s correlation). Shadow shows 95% confidence interval. (C) Genome coverage across the triplicated region in WT, TS, and SAHA-TS neurons. Data are depicted as means ± SEM, with individual mice represented by points. One-way ANOVA, Tukey’s HSD as post hoc; ∗∗∗ p < 0.001. (D) Karyoplot showing the genomic loci of DARs (top, red dots) and DEGs (bottom, red dots). The dotted gray lines indicate the chromosomal breakpoints of the triplicated chromosome in Ts65Dn mice. (E) Representative examples of heterochromatization (ATAC signal IGV tracks, left) and transcriptional rescue (right). Data are depicted as means ± SEM, with individual mice represented by points. One-way ANOVA, Tukey’s HSD as post hoc; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. See also .

    Journal: iScience

    Article Title: HDAC inhibitor treatment restores transcriptome, chromatin accessibility, and memory deficits in a mouse model for Down syndrome

    doi: 10.1016/j.isci.2026.117670

    Figure Lengend Snippet: SAHA transcriptional rescue is mediated by heterochromatization of the triplicated region (A) Venn diagram showing the fraction of triplicated genes whose expression is rescued by SAHA treatment. One-sided Fisher’s exact test. (B) Correlation between the overexpression of triplicated genes and of normalization after SAHA treatment (Pearson’s correlation). Shadow shows 95% confidence interval. (C) Genome coverage across the triplicated region in WT, TS, and SAHA-TS neurons. Data are depicted as means ± SEM, with individual mice represented by points. One-way ANOVA, Tukey’s HSD as post hoc; ∗∗∗ p < 0.001. (D) Karyoplot showing the genomic loci of DARs (top, red dots) and DEGs (bottom, red dots). The dotted gray lines indicate the chromosomal breakpoints of the triplicated chromosome in Ts65Dn mice. (E) Representative examples of heterochromatization (ATAC signal IGV tracks, left) and transcriptional rescue (right). Data are depicted as means ± SEM, with individual mice represented by points. One-way ANOVA, Tukey’s HSD as post hoc; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. See also .

    Article Snippet: Vorinostat (SAHA) , Selleck Chemicals LLC , Cat#S1047.

    Techniques: Expressing, Over Expression

    Journal: iScience

    Article Title: HDAC inhibitor treatment restores transcriptome, chromatin accessibility, and memory deficits in a mouse model for Down syndrome

    doi: 10.1016/j.isci.2026.117670

    Figure Lengend Snippet:

    Article Snippet: Vorinostat (SAHA) , Selleck Chemicals LLC , Cat#S1047.

    Techniques: Cell-Signaling, Recombinant, Bicinchoninic Acid Protein Assay, Isolation, DNA Library Preparation, Software, Analysis

    HDAC2 deficiency or inhibition compromises the antimicrobial efficacy, but improves anti-inflammatory responses in the mice with sepsis. (A-D) Effects of the HDAC2-knockout or inhibition on the survival of mice with CLP-induced or LPS-induced sepsis. Kaplan-Meier curves for the HDAC2-knockout or inhibition by SAHA-treated mice with or CLP-induced or LPS-induced sepsis (n = 20 mice). (E-H) Serum IL-6 and IL-1β levels were determined in the sham or CLP-induced or LPS-induced septic mice treated with or without SAHA (25 mg/kg). These inflammatory parameters were measured by ELISA. Data are shown as mean ± SEM. *p < 0.05; n = 5 mice per group. (I and J) Serum AST, ALT, Urea and Crea levels were measured in sham or CLP-induced or LPS-induced septic mice treated with or without SAHA. Blood was collected by orbital sampling, and these biochemical parameters were measured by the Automatic Biochemistry Analyzer. Data are shown as mean ± SEM. **p < 0.01; n = 5 mice per group.

    Journal: Journal of Advanced Research

    Article Title: HDAC2 enhances the antimicrobial activity of neutrophils by promoting the formation of neutrophil extracellular traps (NETs) in sepsis

    doi: 10.1016/j.jare.2025.08.041

    Figure Lengend Snippet: HDAC2 deficiency or inhibition compromises the antimicrobial efficacy, but improves anti-inflammatory responses in the mice with sepsis. (A-D) Effects of the HDAC2-knockout or inhibition on the survival of mice with CLP-induced or LPS-induced sepsis. Kaplan-Meier curves for the HDAC2-knockout or inhibition by SAHA-treated mice with or CLP-induced or LPS-induced sepsis (n = 20 mice). (E-H) Serum IL-6 and IL-1β levels were determined in the sham or CLP-induced or LPS-induced septic mice treated with or without SAHA (25 mg/kg). These inflammatory parameters were measured by ELISA. Data are shown as mean ± SEM. *p < 0.05; n = 5 mice per group. (I and J) Serum AST, ALT, Urea and Crea levels were measured in sham or CLP-induced or LPS-induced septic mice treated with or without SAHA. Blood was collected by orbital sampling, and these biochemical parameters were measured by the Automatic Biochemistry Analyzer. Data are shown as mean ± SEM. **p < 0.01; n = 5 mice per group.

    Article Snippet: For mouse models of CLP-induced sepsis with HDAC2 inhibition, the animals received an intraperitoneal injection of SAHA (25 mg/kg; MCE, HY-10221) after 0.5 h CLP modeling; For mouse models of LPS-induced sepsis with HDAC2 inhibition, the mice were injected intraperitoneally with LPS (10 mg/kg; Sigma, L4130, derived from E. coli O111:B4) after 1 h injection of SAHA.

    Techniques: Inhibition, Knock-Out, Enzyme-linked Immunosorbent Assay, Sampling

    HDAC2 is required for NET formation. (A and B) Phagocytic uptake and intracellular killing in neutrophils were detected by flow-based assay and colon-formation assay. (A) Phagocytic uptake in neutrophils was detected by flow-based assay. Neutrophils were isolated from peripheral blood of HDAC2 KO or HDAC2 WT mice, and they were co-incubated with E. coli -GFP for two hours. (B) Intracellular killing in neutrophils was detected by colon-formation assay. Blood was taken from the tail vein of the mice, then applied to the pretreated solid MHA medium and incubated at 37 °C for 24 h. The number of bacterial clones was calculated. n = 5 mice per group. (C-D) NETs were detected in the neutrophils from peripheral blood of HDAC2 KO or HDAC2 WT mice by immunofluorescence. Representative data showing MPO-positive cells defined as positive NETs. Data are presented as the means ± SEM. of independent experiments. *P < 0.05, **P < 0.01 (two-tailed Student’s t -test). (E) NETs were detected in the neutrophils from peripheral blood of HDAC2 KO or HDAC2 WT mice by a flow cytometry-based assay. Representative flow data showing positive cells in global Histone H3 citrullination of H3R2, H3R8 or H3R17 sites, defined as positive NETs. (F) NETs markers were detected by western blotting in the neutrophils from HDAC2 WT mice after stimulation with LPS (50 μg/ml) and SAHA (5 μM). Representative data showing H3-Cit expression defined as NETs. The H3 protein was used for western blot loading controls.

    Journal: Journal of Advanced Research

    Article Title: HDAC2 enhances the antimicrobial activity of neutrophils by promoting the formation of neutrophil extracellular traps (NETs) in sepsis

    doi: 10.1016/j.jare.2025.08.041

    Figure Lengend Snippet: HDAC2 is required for NET formation. (A and B) Phagocytic uptake and intracellular killing in neutrophils were detected by flow-based assay and colon-formation assay. (A) Phagocytic uptake in neutrophils was detected by flow-based assay. Neutrophils were isolated from peripheral blood of HDAC2 KO or HDAC2 WT mice, and they were co-incubated with E. coli -GFP for two hours. (B) Intracellular killing in neutrophils was detected by colon-formation assay. Blood was taken from the tail vein of the mice, then applied to the pretreated solid MHA medium and incubated at 37 °C for 24 h. The number of bacterial clones was calculated. n = 5 mice per group. (C-D) NETs were detected in the neutrophils from peripheral blood of HDAC2 KO or HDAC2 WT mice by immunofluorescence. Representative data showing MPO-positive cells defined as positive NETs. Data are presented as the means ± SEM. of independent experiments. *P < 0.05, **P < 0.01 (two-tailed Student’s t -test). (E) NETs were detected in the neutrophils from peripheral blood of HDAC2 KO or HDAC2 WT mice by a flow cytometry-based assay. Representative flow data showing positive cells in global Histone H3 citrullination of H3R2, H3R8 or H3R17 sites, defined as positive NETs. (F) NETs markers were detected by western blotting in the neutrophils from HDAC2 WT mice after stimulation with LPS (50 μg/ml) and SAHA (5 μM). Representative data showing H3-Cit expression defined as NETs. The H3 protein was used for western blot loading controls.

    Article Snippet: For mouse models of CLP-induced sepsis with HDAC2 inhibition, the animals received an intraperitoneal injection of SAHA (25 mg/kg; MCE, HY-10221) after 0.5 h CLP modeling; For mouse models of LPS-induced sepsis with HDAC2 inhibition, the mice were injected intraperitoneally with LPS (10 mg/kg; Sigma, L4130, derived from E. coli O111:B4) after 1 h injection of SAHA.

    Techniques: Tube Formation Assay, Isolation, Incubation, Clone Assay, Immunofluorescence, Two Tailed Test, Flow Cytometry, Western Blot, Expressing

    HDAC2 promotes NETs formation through the acetylation-citrullination pathway. (A–C) Representative images for LPS (50 μg/ml)-stimulated primary neutrophils from HDAC2 WT and HDAC2 KO mice. (A) Immunostaining for histone H3K18 acetylation (green) was performed with DNA counterstained with Hoechst 33342 (blue) and corresponding MFI of quantitative data (E). Scale bars, 20 μm. (B) Immunostaining for histone H3R17 methylation (green) was performed with DNA counterstained with Hoechst 33342 (blue) and corresponding MFI of quantitative data (F). Scale bars, 20 μm. (C) Immunostaining for histone H3R17 citrullination (green) was performed with DNA counterstained with Hoechst 33342 (blue) and corresponding MFI of quantitative data (G). Scale bars, 20 μm. (D) Histone H3R17 citrullination was regulated by H3R17 methylation inhibitor (EZM2302) and HDAC2 inhibitor (SAHA), and immunostaining for histone H3R17 citrullination (green) was performed with DNA counterstained with Hoechst 33342 (blue), the corresponding MFI of quantitative data (H). Scale bars, 20 μm. (I) H3K18 acetylation, H3R17 methylation and H3R17 citrullination were detected by western blotting in the neutrophils from HDAC2 WT and HDAC2 KO mice after stimulation with LPS (50 μg/ml). The H3 protein was used for western blot loading controls. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Journal: Journal of Advanced Research

    Article Title: HDAC2 enhances the antimicrobial activity of neutrophils by promoting the formation of neutrophil extracellular traps (NETs) in sepsis

    doi: 10.1016/j.jare.2025.08.041

    Figure Lengend Snippet: HDAC2 promotes NETs formation through the acetylation-citrullination pathway. (A–C) Representative images for LPS (50 μg/ml)-stimulated primary neutrophils from HDAC2 WT and HDAC2 KO mice. (A) Immunostaining for histone H3K18 acetylation (green) was performed with DNA counterstained with Hoechst 33342 (blue) and corresponding MFI of quantitative data (E). Scale bars, 20 μm. (B) Immunostaining for histone H3R17 methylation (green) was performed with DNA counterstained with Hoechst 33342 (blue) and corresponding MFI of quantitative data (F). Scale bars, 20 μm. (C) Immunostaining for histone H3R17 citrullination (green) was performed with DNA counterstained with Hoechst 33342 (blue) and corresponding MFI of quantitative data (G). Scale bars, 20 μm. (D) Histone H3R17 citrullination was regulated by H3R17 methylation inhibitor (EZM2302) and HDAC2 inhibitor (SAHA), and immunostaining for histone H3R17 citrullination (green) was performed with DNA counterstained with Hoechst 33342 (blue), the corresponding MFI of quantitative data (H). Scale bars, 20 μm. (I) H3K18 acetylation, H3R17 methylation and H3R17 citrullination were detected by western blotting in the neutrophils from HDAC2 WT and HDAC2 KO mice after stimulation with LPS (50 μg/ml). The H3 protein was used for western blot loading controls. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Article Snippet: For mouse models of CLP-induced sepsis with HDAC2 inhibition, the animals received an intraperitoneal injection of SAHA (25 mg/kg; MCE, HY-10221) after 0.5 h CLP modeling; For mouse models of LPS-induced sepsis with HDAC2 inhibition, the mice were injected intraperitoneally with LPS (10 mg/kg; Sigma, L4130, derived from E. coli O111:B4) after 1 h injection of SAHA.

    Techniques: Immunostaining, Methylation, Western Blot

    Protective effects of HDAC2 inhibition and histone methylation inhibition in CLP-induced septic mice (A) Kaplan-Meier curves of CLP-induced septic mice treated with or without SAHA and EZM2302 (n = 20 mice). (B and C) Serum MPO, IL-6 and IL-1β levels were measured with mouse ELISA kit in the CLP-induced septic mice treated with or without SAHA and EZM2302. (D) Serum AST, ALT, Urea and Crea levels were measured in the CLP-induced septic mice treated with or without SAHA and EZM2302. Blood was collected by orbital sampling, and serum biochemical parameters were measured by the Automatic Biochemistry Analyzer. The experiments were performed in quintuplicate, data are presented as the means ± SEM. of independent experiments. *P < 0.05, **P < 0.01 (two-tailed Student’s t -test). (n = 5 mice). (E and F) Histology of lungs, kidneys and livers from mice treated with or without SAHA and EZM2302. (E) The Histology with H&E staining for lungs, kidneys and livers. (F) Cell apoptosis in lungs, kidneys and livers was stained with cleaved-caspase 3. The mice were treated with EZM2302 (25 mg/kg) two hours prior to cecal ligation and puncture (CLP), and SAHA was administered after CLP surgery. SAHA, a HDAC2 inhibitor; EZM2302, a methylation inhibitor.

    Journal: Journal of Advanced Research

    Article Title: HDAC2 enhances the antimicrobial activity of neutrophils by promoting the formation of neutrophil extracellular traps (NETs) in sepsis

    doi: 10.1016/j.jare.2025.08.041

    Figure Lengend Snippet: Protective effects of HDAC2 inhibition and histone methylation inhibition in CLP-induced septic mice (A) Kaplan-Meier curves of CLP-induced septic mice treated with or without SAHA and EZM2302 (n = 20 mice). (B and C) Serum MPO, IL-6 and IL-1β levels were measured with mouse ELISA kit in the CLP-induced septic mice treated with or without SAHA and EZM2302. (D) Serum AST, ALT, Urea and Crea levels were measured in the CLP-induced septic mice treated with or without SAHA and EZM2302. Blood was collected by orbital sampling, and serum biochemical parameters were measured by the Automatic Biochemistry Analyzer. The experiments were performed in quintuplicate, data are presented as the means ± SEM. of independent experiments. *P < 0.05, **P < 0.01 (two-tailed Student’s t -test). (n = 5 mice). (E and F) Histology of lungs, kidneys and livers from mice treated with or without SAHA and EZM2302. (E) The Histology with H&E staining for lungs, kidneys and livers. (F) Cell apoptosis in lungs, kidneys and livers was stained with cleaved-caspase 3. The mice were treated with EZM2302 (25 mg/kg) two hours prior to cecal ligation and puncture (CLP), and SAHA was administered after CLP surgery. SAHA, a HDAC2 inhibitor; EZM2302, a methylation inhibitor.

    Article Snippet: For mouse models of CLP-induced sepsis with HDAC2 inhibition, the animals received an intraperitoneal injection of SAHA (25 mg/kg; MCE, HY-10221) after 0.5 h CLP modeling; For mouse models of LPS-induced sepsis with HDAC2 inhibition, the mice were injected intraperitoneally with LPS (10 mg/kg; Sigma, L4130, derived from E. coli O111:B4) after 1 h injection of SAHA.

    Techniques: Inhibition, Methylation, Enzyme-linked Immunosorbent Assay, Sampling, Two Tailed Test, Staining, Ligation