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eno1 inhibitor ap  (MedChemExpress)


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    MedChemExpress eno1 inhibitor ap
    GPR43 deficiency promotes macrophage M1 polarization via the <t>HIF-1α–ENO1</t> axis. A Representative immunoblots of iNOS and <t>ENO1</t> in WT and Gpr43 −/− <t>BMDMs</t> <t>±</t> <t>AP-III-a4</t> (ENO1 inhibitor, 20 µM) for 6 h. The protein levels are shown in Supplementary Fig. S6A. B , C Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). Representative flow cytometry histogram ( B ) and the iNOS MFI quantification ( C ). D Lactate production in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). E Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). F Kaplan–Meier survival curves for WT and Gpr43 −/− mice after CLP ± AP-III-a4 (10 mg/kg) ( n = 10). G – I Lung histopathology and immunofluorescence after CLP in WT and Gpr43 −/− mice ± AP-III-a4 ( n = 6). Representative H&E and immunofluorescence images ( G , iNOS, green; F4/80, red; nuclei, DAPI, blue). Lung injury scores ( H ) and quantification of iNOS mean fluorescence intensity ( I ). J Representative immunoblots of HIF-1α, c-Myc, p-AKT and p-mTOR expression in M1-polarized WT and Gpr43 −/− BMDMs. The protein levels are shown in Supplementary Fig. S6B. K , L Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± the HIF-1α inhibitor acriflavine (5 μM) for 6 h ( n = 3). Representative histogram of iNOS expression ( K ) and quantification of the iNOS MFI ( L ). M Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± acriflavine ( n = 3). Data are presented as means ± SD. Two-group comparisons used two-tailed unpaired Student’s t -test; multiple groups used one-way ANOVA with Tukey’s post hoc test; survival by log-rank test. Data in C – E and L – M were obtained from three independent experiments. Data in H , I are representative of three independent experiments. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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    Images

    1) Product Images from "GPR43 deficiency aggravates sepsis by promoting gut microbiota–dependent barrier disruption and HIF-1α–ENO1 axis–mediated M1 polarization of macrophages"

    Article Title: GPR43 deficiency aggravates sepsis by promoting gut microbiota–dependent barrier disruption and HIF-1α–ENO1 axis–mediated M1 polarization of macrophages

    Journal: Cellular & Molecular Biology Letters

    doi: 10.1186/s11658-025-00833-4

    GPR43 deficiency promotes macrophage M1 polarization via the HIF-1α–ENO1 axis. A Representative immunoblots of iNOS and ENO1 in WT and Gpr43 −/− BMDMs ± AP-III-a4 (ENO1 inhibitor, 20 µM) for 6 h. The protein levels are shown in Supplementary Fig. S6A. B , C Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). Representative flow cytometry histogram ( B ) and the iNOS MFI quantification ( C ). D Lactate production in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). E Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). F Kaplan–Meier survival curves for WT and Gpr43 −/− mice after CLP ± AP-III-a4 (10 mg/kg) ( n = 10). G – I Lung histopathology and immunofluorescence after CLP in WT and Gpr43 −/− mice ± AP-III-a4 ( n = 6). Representative H&E and immunofluorescence images ( G , iNOS, green; F4/80, red; nuclei, DAPI, blue). Lung injury scores ( H ) and quantification of iNOS mean fluorescence intensity ( I ). J Representative immunoblots of HIF-1α, c-Myc, p-AKT and p-mTOR expression in M1-polarized WT and Gpr43 −/− BMDMs. The protein levels are shown in Supplementary Fig. S6B. K , L Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± the HIF-1α inhibitor acriflavine (5 μM) for 6 h ( n = 3). Representative histogram of iNOS expression ( K ) and quantification of the iNOS MFI ( L ). M Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± acriflavine ( n = 3). Data are presented as means ± SD. Two-group comparisons used two-tailed unpaired Student’s t -test; multiple groups used one-way ANOVA with Tukey’s post hoc test; survival by log-rank test. Data in C – E and L – M were obtained from three independent experiments. Data in H , I are representative of three independent experiments. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
    Figure Legend Snippet: GPR43 deficiency promotes macrophage M1 polarization via the HIF-1α–ENO1 axis. A Representative immunoblots of iNOS and ENO1 in WT and Gpr43 −/− BMDMs ± AP-III-a4 (ENO1 inhibitor, 20 µM) for 6 h. The protein levels are shown in Supplementary Fig. S6A. B , C Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). Representative flow cytometry histogram ( B ) and the iNOS MFI quantification ( C ). D Lactate production in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). E Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). F Kaplan–Meier survival curves for WT and Gpr43 −/− mice after CLP ± AP-III-a4 (10 mg/kg) ( n = 10). G – I Lung histopathology and immunofluorescence after CLP in WT and Gpr43 −/− mice ± AP-III-a4 ( n = 6). Representative H&E and immunofluorescence images ( G , iNOS, green; F4/80, red; nuclei, DAPI, blue). Lung injury scores ( H ) and quantification of iNOS mean fluorescence intensity ( I ). J Representative immunoblots of HIF-1α, c-Myc, p-AKT and p-mTOR expression in M1-polarized WT and Gpr43 −/− BMDMs. The protein levels are shown in Supplementary Fig. S6B. K , L Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± the HIF-1α inhibitor acriflavine (5 μM) for 6 h ( n = 3). Representative histogram of iNOS expression ( K ) and quantification of the iNOS MFI ( L ). M Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± acriflavine ( n = 3). Data are presented as means ± SD. Two-group comparisons used two-tailed unpaired Student’s t -test; multiple groups used one-way ANOVA with Tukey’s post hoc test; survival by log-rank test. Data in C – E and L – M were obtained from three independent experiments. Data in H , I are representative of three independent experiments. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Techniques Used: Western Blot, Flow Cytometry, Expressing, Enzyme-linked Immunosorbent Assay, Histopathology, Immunofluorescence, Fluorescence, Two Tailed Test

    GPR43 expression in patients with sepsis and its correlation with clinical and metabolic markers. A Representative immunoblots (left) and quantification (right) of GPR43 expression in PBMCs from healthy controls and sepsis patients ( n = 36 for sepsis, n = 15 for healthy controls). B qRT–PCR quantification showing GPR43 mRNA expression in PBMCs from sepsis patients compared with healthy controls. C – G Correlation analysis between GPR43 mRNA expression and clinical/metabolic parameters in septic patients, including serum LBP levels ( C ), blood lactate concentrations ( D ), ENO1 mRNA expression ( E ), CRP levels ( F ), and IL-6 mRNA expression ( G ). Data are presented as mean ± SD. Statistical significance in A , B was determined by unpaired Student’s t -test, and correlations in C – G were assessed using Spearman’s correlation test, ** p < 0.01
    Figure Legend Snippet: GPR43 expression in patients with sepsis and its correlation with clinical and metabolic markers. A Representative immunoblots (left) and quantification (right) of GPR43 expression in PBMCs from healthy controls and sepsis patients ( n = 36 for sepsis, n = 15 for healthy controls). B qRT–PCR quantification showing GPR43 mRNA expression in PBMCs from sepsis patients compared with healthy controls. C – G Correlation analysis between GPR43 mRNA expression and clinical/metabolic parameters in septic patients, including serum LBP levels ( C ), blood lactate concentrations ( D ), ENO1 mRNA expression ( E ), CRP levels ( F ), and IL-6 mRNA expression ( G ). Data are presented as mean ± SD. Statistical significance in A , B was determined by unpaired Student’s t -test, and correlations in C – G were assessed using Spearman’s correlation test, ** p < 0.01

    Techniques Used: Expressing, Western Blot, Quantitative RT-PCR



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    GPR43 deficiency promotes macrophage M1 polarization via the <t>HIF-1α–ENO1</t> axis. A Representative immunoblots of iNOS and <t>ENO1</t> in WT and Gpr43 −/− <t>BMDMs</t> <t>±</t> <t>AP-III-a4</t> (ENO1 inhibitor, 20 µM) for 6 h. The protein levels are shown in Supplementary Fig. S6A. B , C Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). Representative flow cytometry histogram ( B ) and the iNOS MFI quantification ( C ). D Lactate production in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). E Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). F Kaplan–Meier survival curves for WT and Gpr43 −/− mice after CLP ± AP-III-a4 (10 mg/kg) ( n = 10). G – I Lung histopathology and immunofluorescence after CLP in WT and Gpr43 −/− mice ± AP-III-a4 ( n = 6). Representative H&E and immunofluorescence images ( G , iNOS, green; F4/80, red; nuclei, DAPI, blue). Lung injury scores ( H ) and quantification of iNOS mean fluorescence intensity ( I ). J Representative immunoblots of HIF-1α, c-Myc, p-AKT and p-mTOR expression in M1-polarized WT and Gpr43 −/− BMDMs. The protein levels are shown in Supplementary Fig. S6B. K , L Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± the HIF-1α inhibitor acriflavine (5 μM) for 6 h ( n = 3). Representative histogram of iNOS expression ( K ) and quantification of the iNOS MFI ( L ). M Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± acriflavine ( n = 3). Data are presented as means ± SD. Two-group comparisons used two-tailed unpaired Student’s t -test; multiple groups used one-way ANOVA with Tukey’s post hoc test; survival by log-rank test. Data in C – E and L – M were obtained from three independent experiments. Data in H , I are representative of three independent experiments. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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    GPR43 deficiency promotes macrophage M1 polarization via the <t>HIF-1α–ENO1</t> axis. A Representative immunoblots of iNOS and <t>ENO1</t> in WT and Gpr43 −/− <t>BMDMs</t> <t>±</t> <t>AP-III-a4</t> (ENO1 inhibitor, 20 µM) for 6 h. The protein levels are shown in Supplementary Fig. S6A. B , C Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). Representative flow cytometry histogram ( B ) and the iNOS MFI quantification ( C ). D Lactate production in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). E Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). F Kaplan–Meier survival curves for WT and Gpr43 −/− mice after CLP ± AP-III-a4 (10 mg/kg) ( n = 10). G – I Lung histopathology and immunofluorescence after CLP in WT and Gpr43 −/− mice ± AP-III-a4 ( n = 6). Representative H&E and immunofluorescence images ( G , iNOS, green; F4/80, red; nuclei, DAPI, blue). Lung injury scores ( H ) and quantification of iNOS mean fluorescence intensity ( I ). J Representative immunoblots of HIF-1α, c-Myc, p-AKT and p-mTOR expression in M1-polarized WT and Gpr43 −/− BMDMs. The protein levels are shown in Supplementary Fig. S6B. K , L Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± the HIF-1α inhibitor acriflavine (5 μM) for 6 h ( n = 3). Representative histogram of iNOS expression ( K ) and quantification of the iNOS MFI ( L ). M Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± acriflavine ( n = 3). Data are presented as means ± SD. Two-group comparisons used two-tailed unpaired Student’s t -test; multiple groups used one-way ANOVA with Tukey’s post hoc test; survival by log-rank test. Data in C – E and L – M were obtained from three independent experiments. Data in H , I are representative of three independent experiments. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
    Eno1 Specific Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    control alpha tubulin  (Proteintech)
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    Proteintech control alpha tubulin
    GPR43 deficiency promotes macrophage M1 polarization via the <t>HIF-1α–ENO1</t> axis. A Representative immunoblots of iNOS and <t>ENO1</t> in WT and Gpr43 −/− <t>BMDMs</t> <t>±</t> <t>AP-III-a4</t> (ENO1 inhibitor, 20 µM) for 6 h. The protein levels are shown in Supplementary Fig. S6A. B , C Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). Representative flow cytometry histogram ( B ) and the iNOS MFI quantification ( C ). D Lactate production in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). E Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). F Kaplan–Meier survival curves for WT and Gpr43 −/− mice after CLP ± AP-III-a4 (10 mg/kg) ( n = 10). G – I Lung histopathology and immunofluorescence after CLP in WT and Gpr43 −/− mice ± AP-III-a4 ( n = 6). Representative H&E and immunofluorescence images ( G , iNOS, green; F4/80, red; nuclei, DAPI, blue). Lung injury scores ( H ) and quantification of iNOS mean fluorescence intensity ( I ). J Representative immunoblots of HIF-1α, c-Myc, p-AKT and p-mTOR expression in M1-polarized WT and Gpr43 −/− BMDMs. The protein levels are shown in Supplementary Fig. S6B. K , L Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± the HIF-1α inhibitor acriflavine (5 μM) for 6 h ( n = 3). Representative histogram of iNOS expression ( K ) and quantification of the iNOS MFI ( L ). M Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± acriflavine ( n = 3). Data are presented as means ± SD. Two-group comparisons used two-tailed unpaired Student’s t -test; multiple groups used one-way ANOVA with Tukey’s post hoc test; survival by log-rank test. Data in C – E and L – M were obtained from three independent experiments. Data in H , I are representative of three independent experiments. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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    333 internal control alpha tubulin  (Proteintech)
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    GPR43 deficiency promotes macrophage M1 polarization via the <t>HIF-1α–ENO1</t> axis. A Representative immunoblots of iNOS and <t>ENO1</t> in WT and Gpr43 −/− <t>BMDMs</t> <t>±</t> <t>AP-III-a4</t> (ENO1 inhibitor, 20 µM) for 6 h. The protein levels are shown in Supplementary Fig. S6A. B , C Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). Representative flow cytometry histogram ( B ) and the iNOS MFI quantification ( C ). D Lactate production in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). E Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). F Kaplan–Meier survival curves for WT and Gpr43 −/− mice after CLP ± AP-III-a4 (10 mg/kg) ( n = 10). G – I Lung histopathology and immunofluorescence after CLP in WT and Gpr43 −/− mice ± AP-III-a4 ( n = 6). Representative H&E and immunofluorescence images ( G , iNOS, green; F4/80, red; nuclei, DAPI, blue). Lung injury scores ( H ) and quantification of iNOS mean fluorescence intensity ( I ). J Representative immunoblots of HIF-1α, c-Myc, p-AKT and p-mTOR expression in M1-polarized WT and Gpr43 −/− BMDMs. The protein levels are shown in Supplementary Fig. S6B. K , L Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± the HIF-1α inhibitor acriflavine (5 μM) for 6 h ( n = 3). Representative histogram of iNOS expression ( K ) and quantification of the iNOS MFI ( L ). M Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± acriflavine ( n = 3). Data are presented as means ± SD. Two-group comparisons used two-tailed unpaired Student’s t -test; multiple groups used one-way ANOVA with Tukey’s post hoc test; survival by log-rank test. Data in C – E and L – M were obtained from three independent experiments. Data in H , I are representative of three independent experiments. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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    Image Search Results


    GPR43 deficiency promotes macrophage M1 polarization via the HIF-1α–ENO1 axis. A Representative immunoblots of iNOS and ENO1 in WT and Gpr43 −/− BMDMs ± AP-III-a4 (ENO1 inhibitor, 20 µM) for 6 h. The protein levels are shown in Supplementary Fig. S6A. B , C Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). Representative flow cytometry histogram ( B ) and the iNOS MFI quantification ( C ). D Lactate production in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). E Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). F Kaplan–Meier survival curves for WT and Gpr43 −/− mice after CLP ± AP-III-a4 (10 mg/kg) ( n = 10). G – I Lung histopathology and immunofluorescence after CLP in WT and Gpr43 −/− mice ± AP-III-a4 ( n = 6). Representative H&E and immunofluorescence images ( G , iNOS, green; F4/80, red; nuclei, DAPI, blue). Lung injury scores ( H ) and quantification of iNOS mean fluorescence intensity ( I ). J Representative immunoblots of HIF-1α, c-Myc, p-AKT and p-mTOR expression in M1-polarized WT and Gpr43 −/− BMDMs. The protein levels are shown in Supplementary Fig. S6B. K , L Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± the HIF-1α inhibitor acriflavine (5 μM) for 6 h ( n = 3). Representative histogram of iNOS expression ( K ) and quantification of the iNOS MFI ( L ). M Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± acriflavine ( n = 3). Data are presented as means ± SD. Two-group comparisons used two-tailed unpaired Student’s t -test; multiple groups used one-way ANOVA with Tukey’s post hoc test; survival by log-rank test. Data in C – E and L – M were obtained from three independent experiments. Data in H , I are representative of three independent experiments. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Journal: Cellular & Molecular Biology Letters

    Article Title: GPR43 deficiency aggravates sepsis by promoting gut microbiota–dependent barrier disruption and HIF-1α–ENO1 axis–mediated M1 polarization of macrophages

    doi: 10.1186/s11658-025-00833-4

    Figure Lengend Snippet: GPR43 deficiency promotes macrophage M1 polarization via the HIF-1α–ENO1 axis. A Representative immunoblots of iNOS and ENO1 in WT and Gpr43 −/− BMDMs ± AP-III-a4 (ENO1 inhibitor, 20 µM) for 6 h. The protein levels are shown in Supplementary Fig. S6A. B , C Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). Representative flow cytometry histogram ( B ) and the iNOS MFI quantification ( C ). D Lactate production in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). E Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± AP-III-a4 ( n = 3). F Kaplan–Meier survival curves for WT and Gpr43 −/− mice after CLP ± AP-III-a4 (10 mg/kg) ( n = 10). G – I Lung histopathology and immunofluorescence after CLP in WT and Gpr43 −/− mice ± AP-III-a4 ( n = 6). Representative H&E and immunofluorescence images ( G , iNOS, green; F4/80, red; nuclei, DAPI, blue). Lung injury scores ( H ) and quantification of iNOS mean fluorescence intensity ( I ). J Representative immunoblots of HIF-1α, c-Myc, p-AKT and p-mTOR expression in M1-polarized WT and Gpr43 −/− BMDMs. The protein levels are shown in Supplementary Fig. S6B. K , L Flow cytometry analysis of iNOS expression in M1-polarized WT and Gpr43 −/− BMDMs ± the HIF-1α inhibitor acriflavine (5 μM) for 6 h ( n = 3). Representative histogram of iNOS expression ( K ) and quantification of the iNOS MFI ( L ). M Supernatant cytokines measured by ELISA in M1-polarized WT and Gpr43 −/− BMDMs ± acriflavine ( n = 3). Data are presented as means ± SD. Two-group comparisons used two-tailed unpaired Student’s t -test; multiple groups used one-way ANOVA with Tukey’s post hoc test; survival by log-rank test. Data in C – E and L – M were obtained from three independent experiments. Data in H , I are representative of three independent experiments. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Article Snippet: For the inhibitor or agonist treatments, BMDMs were pretreated with glycolysis inhibitor 2-deoxyglucose (2-DG) (2 mM, 6 h, MCE, cat. no. HY-13966), ENO1 inhibitor AP-III-a4 (20 μM, 6 h, MCE, cat. no. HY-15858), HIF-1α inhibitor acriflavine (5 μM, 6 h, MCE, cat. no. HY-100575), or the GPR43 agonist TUG-1375 (20 μM, 6 h, MCE, cat. no. HY-112813) before M1 polarization.

    Techniques: Western Blot, Flow Cytometry, Expressing, Enzyme-linked Immunosorbent Assay, Histopathology, Immunofluorescence, Fluorescence, Two Tailed Test

    GPR43 expression in patients with sepsis and its correlation with clinical and metabolic markers. A Representative immunoblots (left) and quantification (right) of GPR43 expression in PBMCs from healthy controls and sepsis patients ( n = 36 for sepsis, n = 15 for healthy controls). B qRT–PCR quantification showing GPR43 mRNA expression in PBMCs from sepsis patients compared with healthy controls. C – G Correlation analysis between GPR43 mRNA expression and clinical/metabolic parameters in septic patients, including serum LBP levels ( C ), blood lactate concentrations ( D ), ENO1 mRNA expression ( E ), CRP levels ( F ), and IL-6 mRNA expression ( G ). Data are presented as mean ± SD. Statistical significance in A , B was determined by unpaired Student’s t -test, and correlations in C – G were assessed using Spearman’s correlation test, ** p < 0.01

    Journal: Cellular & Molecular Biology Letters

    Article Title: GPR43 deficiency aggravates sepsis by promoting gut microbiota–dependent barrier disruption and HIF-1α–ENO1 axis–mediated M1 polarization of macrophages

    doi: 10.1186/s11658-025-00833-4

    Figure Lengend Snippet: GPR43 expression in patients with sepsis and its correlation with clinical and metabolic markers. A Representative immunoblots (left) and quantification (right) of GPR43 expression in PBMCs from healthy controls and sepsis patients ( n = 36 for sepsis, n = 15 for healthy controls). B qRT–PCR quantification showing GPR43 mRNA expression in PBMCs from sepsis patients compared with healthy controls. C – G Correlation analysis between GPR43 mRNA expression and clinical/metabolic parameters in septic patients, including serum LBP levels ( C ), blood lactate concentrations ( D ), ENO1 mRNA expression ( E ), CRP levels ( F ), and IL-6 mRNA expression ( G ). Data are presented as mean ± SD. Statistical significance in A , B was determined by unpaired Student’s t -test, and correlations in C – G were assessed using Spearman’s correlation test, ** p < 0.01

    Article Snippet: For the inhibitor or agonist treatments, BMDMs were pretreated with glycolysis inhibitor 2-deoxyglucose (2-DG) (2 mM, 6 h, MCE, cat. no. HY-13966), ENO1 inhibitor AP-III-a4 (20 μM, 6 h, MCE, cat. no. HY-15858), HIF-1α inhibitor acriflavine (5 μM, 6 h, MCE, cat. no. HY-100575), or the GPR43 agonist TUG-1375 (20 μM, 6 h, MCE, cat. no. HY-112813) before M1 polarization.

    Techniques: Expressing, Western Blot, Quantitative RT-PCR