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HDAC2 is highly expressed in sepsis. (A) Analysis of HDAC2 expression in GEO. HDAC2 expression was analyzed using the GSE95233 dataset, including 22 healthy controls and a total of 102 patients with sepsis. (B)The level of HDAC2 in serum was detected in the <t>CLP-induced</t> septic mice. Blood was collected from mouse orbits, and the level of HDAC2 was measured by Elisa. (C) The level of HDAC2 in serum was detected in <t>the</t> <t>LPS</t> (10 mg/kg)-induced septic mice. Blood was collected from mouse orbits, and the level of HDAC2 was measured by Elisa. (D) The HDAC2 mRNA expression in the peripheral blood leukocytes of (i) CLP-induced septic mice and (ii) 10 mg/kg LPS-induced septic mice. 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 per group.

Clp Modeling, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 201 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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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

Figure Legend Snippet: HDAC2 is highly expressed in sepsis. (A) Analysis of HDAC2 expression in GEO. HDAC2 expression was analyzed using the GSE95233 dataset, including 22 healthy controls and a total of 102 patients with sepsis. (B)The level of HDAC2 in serum was detected in the CLP-induced septic mice. Blood was collected from mouse orbits, and the level of HDAC2 was measured by Elisa. (C) The level of HDAC2 in serum was detected in the LPS (10 mg/kg)-induced septic mice. Blood was collected from mouse orbits, and the level of HDAC2 was measured by Elisa. (D) The HDAC2 mRNA expression in the peripheral blood leukocytes of (i) CLP-induced septic mice and (ii) 10 mg/kg LPS-induced septic mice. 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 per group.

Techniques Used: Expressing, Enzyme-linked Immunosorbent Assay, Two Tailed Test

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

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

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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 highly expressed in sepsis. (A) Analysis of HDAC2 expression in GEO. HDAC2 expression was analyzed using the GSE95233 dataset, including 22 healthy controls and a total of 102 patients with sepsis. (B)The level of HDAC2 in serum was detected in the CLP-induced septic mice. Blood was collected from mouse orbits, and the level of HDAC2 was measured by Elisa. (C) The level of HDAC2 in serum was detected in the LPS (10 mg/kg)-induced septic mice. Blood was collected from mouse orbits, and the level of HDAC2 was measured by Elisa. (D) The HDAC2 mRNA expression in the peripheral blood leukocytes of (i) CLP-induced septic mice and (ii) 10 mg/kg LPS-induced septic mice. 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 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: Expressing, Enzyme-linked Immunosorbent Assay, Two Tailed Test

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.

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

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.

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

Lack of SIRT1 activity exacerbate sepsis-induced ALI and sepsis severity. (A) Histologic analysis of lung tissues (scale bars, 50 μm). (B) Lung injury score. (C) Representative blots. (D) SIRT1 expression in lung tissue. (E) Relative SIRT1 activity in lung tissue. (F) Histologic analysis of hearts, liver, and kidney tissues (scale bars, 50 μm). (G) Representative in situ detection of lung parenchymal cell apoptosis and endothelial cell apoptosis by TUNEL staining (red) and CD31 (green) (scale bars, 50 μm). (H) Percentage of TUNEL-positive nuclei. (I) Percentage of TUNEL-positive endothelial cells. (J) Lung MPO activity. (K) Survival after cecal ligation and puncture (CLP) ( n =12). (L) Rectal temperature. (M) Weight loss after CLP. n =8 in each group except for survival analysis. The data shown in (B)–(E), (I)–(J), and (L)–(M) represent means±SD. Statistical significance was tested using one-way ANOVA with post-hoc Bonferroni correction in (B), (D)–(E), (H)–(J), and (L)–(M). The Kaplan–Meier method was used followed by a log-rank (Mantel-Cox) test in (K).

Journal: International Journal of Surgery (London, England)

Article Title: SIRT1-Rab7 axis attenuates NLRP3 and STING activation through late endosomal-dependent mitophagy during sepsis-induced acute lung injury

doi: 10.1097/JS9.0000000000001215

Figure Lengend Snippet: Lack of SIRT1 activity exacerbate sepsis-induced ALI and sepsis severity. (A) Histologic analysis of lung tissues (scale bars, 50 μm). (B) Lung injury score. (C) Representative blots. (D) SIRT1 expression in lung tissue. (E) Relative SIRT1 activity in lung tissue. (F) Histologic analysis of hearts, liver, and kidney tissues (scale bars, 50 μm). (G) Representative in situ detection of lung parenchymal cell apoptosis and endothelial cell apoptosis by TUNEL staining (red) and CD31 (green) (scale bars, 50 μm). (H) Percentage of TUNEL-positive nuclei. (I) Percentage of TUNEL-positive endothelial cells. (J) Lung MPO activity. (K) Survival after cecal ligation and puncture (CLP) ( n =12). (L) Rectal temperature. (M) Weight loss after CLP. n =8 in each group except for survival analysis. The data shown in (B)–(E), (I)–(J), and (L)–(M) represent means±SD. Statistical significance was tested using one-way ANOVA with post-hoc Bonferroni correction in (B), (D)–(E), (H)–(J), and (L)–(M). The Kaplan–Meier method was used followed by a log-rank (Mantel-Cox) test in (K).

Article Snippet: To understand the therapeutic potential of NLRP3 targeting in SIRT1 deficiency following CLP models surgery, MCC950 (50 mg/kg, MedChemExpress) were administered intraperitoneally at 1 h before the CLP surgery .

Techniques: Activity Assay, Expressing, In Situ, TUNEL Assay, Staining, Ligation

Pharmacological inhibition of cGAS-STING and NLRP3 reduces lack of SIRT1 activity-induced lung endotheliopathy and sepsis severity in mice models with sepsis. (A) Representative blots. (B) pSTING expression. (C) GSDMD expression. (D) NLRP3 expression. (E) VCAM1 expression. (F) Histologic analysis of lung tissues (scale bars, 50 μm). (G) Lung injury score (medians, interquartile range). (H) lung MPO activity. (I) Evans blue dye leakage in ears ( n =5). (J) Quantitative analysis of the amount of extravasated Evans blue dye from mouse ears. §§ P <0.01 versus Con, ## P <0.01 versus CLP, ** P <0.01 versus CLP+EX527. n =8 in each group except for Evans blue dye leakage in ears. The data represent means±SD. Statistical significance was tested using one-way ANOVA with post-hoc Bonferroni correction.

Journal: International Journal of Surgery (London, England)

Article Title: SIRT1-Rab7 axis attenuates NLRP3 and STING activation through late endosomal-dependent mitophagy during sepsis-induced acute lung injury

doi: 10.1097/JS9.0000000000001215

Figure Lengend Snippet: Pharmacological inhibition of cGAS-STING and NLRP3 reduces lack of SIRT1 activity-induced lung endotheliopathy and sepsis severity in mice models with sepsis. (A) Representative blots. (B) pSTING expression. (C) GSDMD expression. (D) NLRP3 expression. (E) VCAM1 expression. (F) Histologic analysis of lung tissues (scale bars, 50 μm). (G) Lung injury score (medians, interquartile range). (H) lung MPO activity. (I) Evans blue dye leakage in ears ( n =5). (J) Quantitative analysis of the amount of extravasated Evans blue dye from mouse ears. §§ P <0.01 versus Con, ## P <0.01 versus CLP, ** P <0.01 versus CLP+EX527. n =8 in each group except for Evans blue dye leakage in ears. The data represent means±SD. Statistical significance was tested using one-way ANOVA with post-hoc Bonferroni correction.

Techniques: Inhibition, Activity Assay, Expressing

Journal: International Journal of Surgery (London, England)

Article Title: SIRT1-Rab7 axis attenuates NLRP3 and STING activation through late endosomal-dependent mitophagy during sepsis-induced acute lung injury

doi: 10.1097/JS9.0000000000001215

Figure Lengend Snippet: Pharmacological inhibition of cGAS-STING and NLRP3 reduces lack of SIRT1 activity-induced lung endotheliopathy and sepsis severity in mice models with sepsis. (A) Survival after cecal ligation and puncture (CLP) ( n =12). (B) Rectal temperature. (C) Weight loss after CLP. (D) Serum concentrations of IL-β. (E) Serum concentrations of IL-6. (F) Serum concentrations of TNF-α. ** P <0.01 versus CLP+EX527. n =8 in each group except for survival analysis. The data represent means±SD in (B)–(F). Statistical significance was tested using one-way ANOVA with post-hoc Bonferroni correction in (B)–(F). The Kaplan–Meier method was used followed by a log-rank (Mantel-Cox) test in (A).

Techniques: Inhibition, Activity Assay, Ligation

Pharmacological restoration of SIRT1 activity ameliorated lung endotheliopathy and sepsis severity in mouse models of sepsis. (A) Representative blots. (B) pSTING expression. (C) GSDMD expression. (D) NLRP3 expression. (E) p62 expression. (F) VCAM1 expression. (G) Serum concentrations of Angpt2. (H) lung MPO activity. (I) Histologic analysis of lung tissues (scale bars, 50 μm). (J) Lung injury score. (K) Survival after cecal ligation and puncture (CLP) ( n =12). (L) Rectal temperature loss at 12 h. (M) Weight loss after CLP. # P <0.05 versus CLP, ## P <0.01 versus CLP, ** P <0.01 versus CLP+SRT1720. n =8 in each group except for survival analysis. The data represent means±SD in (B)–(H), (J), (L), and (M). Statistical significance was tested using one-way ANOVA with post-hoc Bonferroni correction (A)–(J), (L), and (M). The Kaplan–Meier method was used followed by a log-rank (Mantel-Cox) test in (K).

Journal: International Journal of Surgery (London, England)

Article Title: SIRT1-Rab7 axis attenuates NLRP3 and STING activation through late endosomal-dependent mitophagy during sepsis-induced acute lung injury

doi: 10.1097/JS9.0000000000001215

Figure Lengend Snippet: Pharmacological restoration of SIRT1 activity ameliorated lung endotheliopathy and sepsis severity in mouse models of sepsis. (A) Representative blots. (B) pSTING expression. (C) GSDMD expression. (D) NLRP3 expression. (E) p62 expression. (F) VCAM1 expression. (G) Serum concentrations of Angpt2. (H) lung MPO activity. (I) Histologic analysis of lung tissues (scale bars, 50 μm). (J) Lung injury score. (K) Survival after cecal ligation and puncture (CLP) ( n =12). (L) Rectal temperature loss at 12 h. (M) Weight loss after CLP. # P <0.05 versus CLP, ## P <0.01 versus CLP, ** P <0.01 versus CLP+SRT1720. n =8 in each group except for survival analysis. The data represent means±SD in (B)–(H), (J), (L), and (M). Statistical significance was tested using one-way ANOVA with post-hoc Bonferroni correction (A)–(J), (L), and (M). The Kaplan–Meier method was used followed by a log-rank (Mantel-Cox) test in (K).

Techniques: Activity Assay, Expressing, Ligation

Pharmacological restoration of SIRT1 activity ameliorated lung endotheliopathy and sepsis severity in mouse models of sepsis. (A) Serum concentrations of angiopoietin 2 (Angpt2). (B) Representative blots. (C) VCAM1 expression. (D) Histologic analysis of lung tissues (scale bars, 50 μm). (E) Lung injury score. (F) Lung MPO activity. (G) Rectal temperature. (H) Weight loss after CLP. (I) Serum concentrations of IL-β. (J) Serum concentrations of IL-6. (K) Serum concentrations of TNF-α. n =5 in each group. The data represent means±SD. Statistical significance was tested using one-way ANOVA with post-hoc Bonferroni correction.

Journal: International Journal of Surgery (London, England)

Article Title: SIRT1-Rab7 axis attenuates NLRP3 and STING activation through late endosomal-dependent mitophagy during sepsis-induced acute lung injury

doi: 10.1097/JS9.0000000000001215

Figure Lengend Snippet: Pharmacological restoration of SIRT1 activity ameliorated lung endotheliopathy and sepsis severity in mouse models of sepsis. (A) Serum concentrations of angiopoietin 2 (Angpt2). (B) Representative blots. (C) VCAM1 expression. (D) Histologic analysis of lung tissues (scale bars, 50 μm). (E) Lung injury score. (F) Lung MPO activity. (G) Rectal temperature. (H) Weight loss after CLP. (I) Serum concentrations of IL-β. (J) Serum concentrations of IL-6. (K) Serum concentrations of TNF-α. n =5 in each group. The data represent means±SD. Statistical significance was tested using one-way ANOVA with post-hoc Bonferroni correction.

Techniques: Activity Assay, Expressing

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