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sirt2  (MedChemExpress)


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    Structured Review

    MedChemExpress sirt2
    Primer Sequences for Real‐Time PCR Analysis
    Sirt2, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sirt2/product/MedChemExpress
    Average 92 stars, based on 2 article reviews
    sirt2 - by Bioz Stars, 2026-02
    92/100 stars

    Images

    1) Product Images from "Colchicine Ameliorates Dilated Cardiomyopathy Via SIRT2 ‐Mediated Suppression of NLRP3 Inflammasome Activation"

    Article Title: Colchicine Ameliorates Dilated Cardiomyopathy Via SIRT2 ‐Mediated Suppression of NLRP3 Inflammasome Activation

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    doi: 10.1161/JAHA.122.025266

    Primer Sequences for Real‐Time PCR Analysis
    Figure Legend Snippet: Primer Sequences for Real‐Time PCR Analysis

    Techniques Used: Real-time Polymerase Chain Reaction

    A , Acetylated NLRP3 (NOD‐like receptor protein 3) levels in the cardiac tissues of mice at the end point of experiment. Immunoglobulin G is the negative control and GAPDH is the input loading control. Data are representative of 3 independent experiments. Western blot analysis on expression of SIRT2 in cardiac tissues at the end of experiment (n=6 each group) on the right. B , Relative expression of SIRT2 mRNA is normalized to GAPDH mRNA in cardiac tissues (n=4 each group). C , Relative expression of inflammatory cytokine interleukin‐1 mRNA and NLRP3 mRNA are normalized to GAPDH mRNA in primary neutrophil that are treated +/− colchicine (10 μmol/L, 2 hours), +/− SIRT2 inhibitor AGK2 (10 μmol/L, 2 hours) or challenged with doxorubicin (5 μmol/L, 2 hours) and inflammasome activators nigericin (10 μmol/L, 2 hours); n=6 each group. D , Western blot analysis on expression of NLRP3 inflammasome pathway in primary neutrophil that are treated +/− colchicine (10 μmol/L, 2 hours), +/− SIRT2 inhibitor AGK2 (10 μmol/L, 2 hours) or challenged with doxorubicin (5 μmol/L, 2 hours) and inflammasome activators nigericin (10 μmol/L, 2 hours). GAPDH shows loading control. Data are representative of 3 independent experiments. Data are shown as mean±SEM. Data of ( A and B ) are analyzed by 1‐way ANOVA (Tukey post‐test). Data of ( C and D ) are analyzed by 2‐way ANOVA (Bonferroni post‐test). DCM indicates dilated cardiomyopathy; IL‐1β, interleukin‐1β; NLRP3, NOD‐like receptor protein 3; and SIRT2, Sirtuin 2. * P <0.05 between groups; ** P <0.01 between groups; *** P <0.005 between groups; and **** P <0.001 between groups. AGK2 indicates a reversible inhibitor of SIRT2; AIM2, absent in melanoma 2; ASC, apoptosis‐associated speck‐like protein with CARD domain; Col, colchicine; IB, immunoblot; IP, immunoprecipitation; Ly6G, lymphocyte antigen 6 complex locus G6D.
    Figure Legend Snippet: A , Acetylated NLRP3 (NOD‐like receptor protein 3) levels in the cardiac tissues of mice at the end point of experiment. Immunoglobulin G is the negative control and GAPDH is the input loading control. Data are representative of 3 independent experiments. Western blot analysis on expression of SIRT2 in cardiac tissues at the end of experiment (n=6 each group) on the right. B , Relative expression of SIRT2 mRNA is normalized to GAPDH mRNA in cardiac tissues (n=4 each group). C , Relative expression of inflammatory cytokine interleukin‐1 mRNA and NLRP3 mRNA are normalized to GAPDH mRNA in primary neutrophil that are treated +/− colchicine (10 μmol/L, 2 hours), +/− SIRT2 inhibitor AGK2 (10 μmol/L, 2 hours) or challenged with doxorubicin (5 μmol/L, 2 hours) and inflammasome activators nigericin (10 μmol/L, 2 hours); n=6 each group. D , Western blot analysis on expression of NLRP3 inflammasome pathway in primary neutrophil that are treated +/− colchicine (10 μmol/L, 2 hours), +/− SIRT2 inhibitor AGK2 (10 μmol/L, 2 hours) or challenged with doxorubicin (5 μmol/L, 2 hours) and inflammasome activators nigericin (10 μmol/L, 2 hours). GAPDH shows loading control. Data are representative of 3 independent experiments. Data are shown as mean±SEM. Data of ( A and B ) are analyzed by 1‐way ANOVA (Tukey post‐test). Data of ( C and D ) are analyzed by 2‐way ANOVA (Bonferroni post‐test). DCM indicates dilated cardiomyopathy; IL‐1β, interleukin‐1β; NLRP3, NOD‐like receptor protein 3; and SIRT2, Sirtuin 2. * P <0.05 between groups; ** P <0.01 between groups; *** P <0.005 between groups; and **** P <0.001 between groups. AGK2 indicates a reversible inhibitor of SIRT2; AIM2, absent in melanoma 2; ASC, apoptosis‐associated speck‐like protein with CARD domain; Col, colchicine; IB, immunoblot; IP, immunoprecipitation; Ly6G, lymphocyte antigen 6 complex locus G6D.

    Techniques Used: Negative Control, Western Blot, Expressing, Immunoprecipitation

    A , Representative immunofluorescence images of cardiac tissues staining with NLRP3 (green), SIRT2 (red), and DAPI (blue). (n=6–8 each group). Five images per mouse are evaluated. Scale bar=50 μm. B , Representative immunofluorescence images of primary neutrophils that are treated +/− colchicine (10 μmol/L, 2 hours), +/− SIRT2 inhibitor AGK2 (10 μmol/L, 2 hours) or challenged with doxorubicin (5 μmol/L, 2 hours) and inflammasome activators nigericin (10 μmol/L, 2 hours). NLRP3 (green), SIRT2 (red) and DAPI (blue). Scale bar=20 μm. Data are representative of 3 independent experiments. C , The effect of SIRT2 on the deacetylation of NLRP3 is evaluated by coimmunoprecipitation. NLRP3‐Flag plasmid is transfected into NB4 cell line, then NB4 cell line is treated with +/− colchicine (10 μmol/L, 2 hours), +/− SIRT2 inhibitor AGK2 (10 μmol/L, 2 hours) or challenged with doxorubicin (5 μmol/L, 2 hours) and inflammasome activators nigericin (10 μmol/L, 2 hours). Cell lysates are immunopurified with anti‐Flag antibody. Then the expression of acetylated lysine is measured by IP. GAPDH is the input loading control. Data are representative of 3 independent experiments. DCM indicates dilated cardiomyopathy; IL‐1β, interleukin‐1β; NLRP3, NOD‐like receptor protein 3; and SIRT2, Sirtuin 2. AGK2, a reversible inhibitor of SIRT2; Col, colchicine; IB, immunoblot; IP, Immunoprecipitation.
    Figure Legend Snippet: A , Representative immunofluorescence images of cardiac tissues staining with NLRP3 (green), SIRT2 (red), and DAPI (blue). (n=6–8 each group). Five images per mouse are evaluated. Scale bar=50 μm. B , Representative immunofluorescence images of primary neutrophils that are treated +/− colchicine (10 μmol/L, 2 hours), +/− SIRT2 inhibitor AGK2 (10 μmol/L, 2 hours) or challenged with doxorubicin (5 μmol/L, 2 hours) and inflammasome activators nigericin (10 μmol/L, 2 hours). NLRP3 (green), SIRT2 (red) and DAPI (blue). Scale bar=20 μm. Data are representative of 3 independent experiments. C , The effect of SIRT2 on the deacetylation of NLRP3 is evaluated by coimmunoprecipitation. NLRP3‐Flag plasmid is transfected into NB4 cell line, then NB4 cell line is treated with +/− colchicine (10 μmol/L, 2 hours), +/− SIRT2 inhibitor AGK2 (10 μmol/L, 2 hours) or challenged with doxorubicin (5 μmol/L, 2 hours) and inflammasome activators nigericin (10 μmol/L, 2 hours). Cell lysates are immunopurified with anti‐Flag antibody. Then the expression of acetylated lysine is measured by IP. GAPDH is the input loading control. Data are representative of 3 independent experiments. DCM indicates dilated cardiomyopathy; IL‐1β, interleukin‐1β; NLRP3, NOD‐like receptor protein 3; and SIRT2, Sirtuin 2. AGK2, a reversible inhibitor of SIRT2; Col, colchicine; IB, immunoblot; IP, Immunoprecipitation.

    Techniques Used: Immunofluorescence, Staining, Plasmid Preparation, Transfection, Expressing, Western Blot, Immunoprecipitation

    A through C , Cardiac function is analyzed by 2‐dimensional murine echocardiography, left ventricular (LV) ejection fraction, LV fractional shortening, LV internal dimensions at end‐diastole, and LV internal dimensions at end‐systole values are measured at the end point of experiment (n=10 each group). D , Kaplan–Meier survival curve for each group mice followed for 4 weeks with or without doxorubicin challenge (n=25 each group). E , The changes of body weight from beginning to end (n=10 each group). F , Relative expression of ANP (atrial natriuretic peptide) mRNA and BNP (brain natriuretic peptide) mRNA are normalized to GAPDH mRNA in murine cardiac tissues at the end point of experiment. G and H , The representative hematoxylin and eosin staining ( G ) and Sirius red staining ( H ) of hearts in each group are shown. Quantification of interstitial fibrosis (% area) in hearts is shown on the right; n=8 each group. Five images per mouse are evaluated. Scale bar=50 μm. Data are shown as mean±SEM. Data of ( B , C , and E through G ) are analyzed by 1‐way ANOVA (Tukey post‐test). Data of ( D ) is analyzed by Mantel‐Cox test. ANP indicates atrial natriuretic peptide; BNP, brain natriuretic peptide; DCM, dilated cardiomyopathy; LVEF, left ventricular ejection fraction; LVFS, left ventricular fractional shortening; LVIDd, left ventricular internal dimensions at end‐diastole; and LVIDs, left ventricular internal dimensions at end‐systole. * P <0.05 between groups; ** P <0.01 between groups; *** P <0.005 between groups and **** P <0.001 between groups. AGK2 indicates a reversible inhibitor of SIRT2; Col, colchicine.
    Figure Legend Snippet: A through C , Cardiac function is analyzed by 2‐dimensional murine echocardiography, left ventricular (LV) ejection fraction, LV fractional shortening, LV internal dimensions at end‐diastole, and LV internal dimensions at end‐systole values are measured at the end point of experiment (n=10 each group). D , Kaplan–Meier survival curve for each group mice followed for 4 weeks with or without doxorubicin challenge (n=25 each group). E , The changes of body weight from beginning to end (n=10 each group). F , Relative expression of ANP (atrial natriuretic peptide) mRNA and BNP (brain natriuretic peptide) mRNA are normalized to GAPDH mRNA in murine cardiac tissues at the end point of experiment. G and H , The representative hematoxylin and eosin staining ( G ) and Sirius red staining ( H ) of hearts in each group are shown. Quantification of interstitial fibrosis (% area) in hearts is shown on the right; n=8 each group. Five images per mouse are evaluated. Scale bar=50 μm. Data are shown as mean±SEM. Data of ( B , C , and E through G ) are analyzed by 1‐way ANOVA (Tukey post‐test). Data of ( D ) is analyzed by Mantel‐Cox test. ANP indicates atrial natriuretic peptide; BNP, brain natriuretic peptide; DCM, dilated cardiomyopathy; LVEF, left ventricular ejection fraction; LVFS, left ventricular fractional shortening; LVIDd, left ventricular internal dimensions at end‐diastole; and LVIDs, left ventricular internal dimensions at end‐systole. * P <0.05 between groups; ** P <0.01 between groups; *** P <0.005 between groups and **** P <0.001 between groups. AGK2 indicates a reversible inhibitor of SIRT2; Col, colchicine.

    Techniques Used: Expressing, Staining



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    sirt2  (MedChemExpress)
    92
    MedChemExpress sirt2
    Primer Sequences for Real‐Time PCR Analysis
    Sirt2, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sirt2/product/MedChemExpress
    Average 92 stars, based on 1 article reviews
    sirt2 - by Bioz Stars, 2026-02
    92/100 stars
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    Primer Sequences for Real‐Time PCR Analysis

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Colchicine Ameliorates Dilated Cardiomyopathy Via SIRT2 ‐Mediated Suppression of NLRP3 Inflammasome Activation

    doi: 10.1161/JAHA.122.025266

    Figure Lengend Snippet: Primer Sequences for Real‐Time PCR Analysis

    Article Snippet: To identify the role of SIRT2, the SIRT2 inhibitor AGK2 (10 μmol/L, MCE, NJ, USA) was added to RPMI 1640 medium for 4 hours.

    Techniques: Real-time Polymerase Chain Reaction

    A , Acetylated NLRP3 (NOD‐like receptor protein 3) levels in the cardiac tissues of mice at the end point of experiment. Immunoglobulin G is the negative control and GAPDH is the input loading control. Data are representative of 3 independent experiments. Western blot analysis on expression of SIRT2 in cardiac tissues at the end of experiment (n=6 each group) on the right. B , Relative expression of SIRT2 mRNA is normalized to GAPDH mRNA in cardiac tissues (n=4 each group). C , Relative expression of inflammatory cytokine interleukin‐1 mRNA and NLRP3 mRNA are normalized to GAPDH mRNA in primary neutrophil that are treated +/− colchicine (10 μmol/L, 2 hours), +/− SIRT2 inhibitor AGK2 (10 μmol/L, 2 hours) or challenged with doxorubicin (5 μmol/L, 2 hours) and inflammasome activators nigericin (10 μmol/L, 2 hours); n=6 each group. D , Western blot analysis on expression of NLRP3 inflammasome pathway in primary neutrophil that are treated +/− colchicine (10 μmol/L, 2 hours), +/− SIRT2 inhibitor AGK2 (10 μmol/L, 2 hours) or challenged with doxorubicin (5 μmol/L, 2 hours) and inflammasome activators nigericin (10 μmol/L, 2 hours). GAPDH shows loading control. Data are representative of 3 independent experiments. Data are shown as mean±SEM. Data of ( A and B ) are analyzed by 1‐way ANOVA (Tukey post‐test). Data of ( C and D ) are analyzed by 2‐way ANOVA (Bonferroni post‐test). DCM indicates dilated cardiomyopathy; IL‐1β, interleukin‐1β; NLRP3, NOD‐like receptor protein 3; and SIRT2, Sirtuin 2. * P <0.05 between groups; ** P <0.01 between groups; *** P <0.005 between groups; and **** P <0.001 between groups. AGK2 indicates a reversible inhibitor of SIRT2; AIM2, absent in melanoma 2; ASC, apoptosis‐associated speck‐like protein with CARD domain; Col, colchicine; IB, immunoblot; IP, immunoprecipitation; Ly6G, lymphocyte antigen 6 complex locus G6D.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Colchicine Ameliorates Dilated Cardiomyopathy Via SIRT2 ‐Mediated Suppression of NLRP3 Inflammasome Activation

    doi: 10.1161/JAHA.122.025266

    Figure Lengend Snippet: A , Acetylated NLRP3 (NOD‐like receptor protein 3) levels in the cardiac tissues of mice at the end point of experiment. Immunoglobulin G is the negative control and GAPDH is the input loading control. Data are representative of 3 independent experiments. Western blot analysis on expression of SIRT2 in cardiac tissues at the end of experiment (n=6 each group) on the right. B , Relative expression of SIRT2 mRNA is normalized to GAPDH mRNA in cardiac tissues (n=4 each group). C , Relative expression of inflammatory cytokine interleukin‐1 mRNA and NLRP3 mRNA are normalized to GAPDH mRNA in primary neutrophil that are treated +/− colchicine (10 μmol/L, 2 hours), +/− SIRT2 inhibitor AGK2 (10 μmol/L, 2 hours) or challenged with doxorubicin (5 μmol/L, 2 hours) and inflammasome activators nigericin (10 μmol/L, 2 hours); n=6 each group. D , Western blot analysis on expression of NLRP3 inflammasome pathway in primary neutrophil that are treated +/− colchicine (10 μmol/L, 2 hours), +/− SIRT2 inhibitor AGK2 (10 μmol/L, 2 hours) or challenged with doxorubicin (5 μmol/L, 2 hours) and inflammasome activators nigericin (10 μmol/L, 2 hours). GAPDH shows loading control. Data are representative of 3 independent experiments. Data are shown as mean±SEM. Data of ( A and B ) are analyzed by 1‐way ANOVA (Tukey post‐test). Data of ( C and D ) are analyzed by 2‐way ANOVA (Bonferroni post‐test). DCM indicates dilated cardiomyopathy; IL‐1β, interleukin‐1β; NLRP3, NOD‐like receptor protein 3; and SIRT2, Sirtuin 2. * P <0.05 between groups; ** P <0.01 between groups; *** P <0.005 between groups; and **** P <0.001 between groups. AGK2 indicates a reversible inhibitor of SIRT2; AIM2, absent in melanoma 2; ASC, apoptosis‐associated speck‐like protein with CARD domain; Col, colchicine; IB, immunoblot; IP, immunoprecipitation; Ly6G, lymphocyte antigen 6 complex locus G6D.

    Article Snippet: To identify the role of SIRT2, the SIRT2 inhibitor AGK2 (10 μmol/L, MCE, NJ, USA) was added to RPMI 1640 medium for 4 hours.

    Techniques: Negative Control, Western Blot, Expressing, Immunoprecipitation

    A , Representative immunofluorescence images of cardiac tissues staining with NLRP3 (green), SIRT2 (red), and DAPI (blue). (n=6–8 each group). Five images per mouse are evaluated. Scale bar=50 μm. B , Representative immunofluorescence images of primary neutrophils that are treated +/− colchicine (10 μmol/L, 2 hours), +/− SIRT2 inhibitor AGK2 (10 μmol/L, 2 hours) or challenged with doxorubicin (5 μmol/L, 2 hours) and inflammasome activators nigericin (10 μmol/L, 2 hours). NLRP3 (green), SIRT2 (red) and DAPI (blue). Scale bar=20 μm. Data are representative of 3 independent experiments. C , The effect of SIRT2 on the deacetylation of NLRP3 is evaluated by coimmunoprecipitation. NLRP3‐Flag plasmid is transfected into NB4 cell line, then NB4 cell line is treated with +/− colchicine (10 μmol/L, 2 hours), +/− SIRT2 inhibitor AGK2 (10 μmol/L, 2 hours) or challenged with doxorubicin (5 μmol/L, 2 hours) and inflammasome activators nigericin (10 μmol/L, 2 hours). Cell lysates are immunopurified with anti‐Flag antibody. Then the expression of acetylated lysine is measured by IP. GAPDH is the input loading control. Data are representative of 3 independent experiments. DCM indicates dilated cardiomyopathy; IL‐1β, interleukin‐1β; NLRP3, NOD‐like receptor protein 3; and SIRT2, Sirtuin 2. AGK2, a reversible inhibitor of SIRT2; Col, colchicine; IB, immunoblot; IP, Immunoprecipitation.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Colchicine Ameliorates Dilated Cardiomyopathy Via SIRT2 ‐Mediated Suppression of NLRP3 Inflammasome Activation

    doi: 10.1161/JAHA.122.025266

    Figure Lengend Snippet: A , Representative immunofluorescence images of cardiac tissues staining with NLRP3 (green), SIRT2 (red), and DAPI (blue). (n=6–8 each group). Five images per mouse are evaluated. Scale bar=50 μm. B , Representative immunofluorescence images of primary neutrophils that are treated +/− colchicine (10 μmol/L, 2 hours), +/− SIRT2 inhibitor AGK2 (10 μmol/L, 2 hours) or challenged with doxorubicin (5 μmol/L, 2 hours) and inflammasome activators nigericin (10 μmol/L, 2 hours). NLRP3 (green), SIRT2 (red) and DAPI (blue). Scale bar=20 μm. Data are representative of 3 independent experiments. C , The effect of SIRT2 on the deacetylation of NLRP3 is evaluated by coimmunoprecipitation. NLRP3‐Flag plasmid is transfected into NB4 cell line, then NB4 cell line is treated with +/− colchicine (10 μmol/L, 2 hours), +/− SIRT2 inhibitor AGK2 (10 μmol/L, 2 hours) or challenged with doxorubicin (5 μmol/L, 2 hours) and inflammasome activators nigericin (10 μmol/L, 2 hours). Cell lysates are immunopurified with anti‐Flag antibody. Then the expression of acetylated lysine is measured by IP. GAPDH is the input loading control. Data are representative of 3 independent experiments. DCM indicates dilated cardiomyopathy; IL‐1β, interleukin‐1β; NLRP3, NOD‐like receptor protein 3; and SIRT2, Sirtuin 2. AGK2, a reversible inhibitor of SIRT2; Col, colchicine; IB, immunoblot; IP, Immunoprecipitation.

    Article Snippet: To identify the role of SIRT2, the SIRT2 inhibitor AGK2 (10 μmol/L, MCE, NJ, USA) was added to RPMI 1640 medium for 4 hours.

    Techniques: Immunofluorescence, Staining, Plasmid Preparation, Transfection, Expressing, Western Blot, Immunoprecipitation

    A through C , Cardiac function is analyzed by 2‐dimensional murine echocardiography, left ventricular (LV) ejection fraction, LV fractional shortening, LV internal dimensions at end‐diastole, and LV internal dimensions at end‐systole values are measured at the end point of experiment (n=10 each group). D , Kaplan–Meier survival curve for each group mice followed for 4 weeks with or without doxorubicin challenge (n=25 each group). E , The changes of body weight from beginning to end (n=10 each group). F , Relative expression of ANP (atrial natriuretic peptide) mRNA and BNP (brain natriuretic peptide) mRNA are normalized to GAPDH mRNA in murine cardiac tissues at the end point of experiment. G and H , The representative hematoxylin and eosin staining ( G ) and Sirius red staining ( H ) of hearts in each group are shown. Quantification of interstitial fibrosis (% area) in hearts is shown on the right; n=8 each group. Five images per mouse are evaluated. Scale bar=50 μm. Data are shown as mean±SEM. Data of ( B , C , and E through G ) are analyzed by 1‐way ANOVA (Tukey post‐test). Data of ( D ) is analyzed by Mantel‐Cox test. ANP indicates atrial natriuretic peptide; BNP, brain natriuretic peptide; DCM, dilated cardiomyopathy; LVEF, left ventricular ejection fraction; LVFS, left ventricular fractional shortening; LVIDd, left ventricular internal dimensions at end‐diastole; and LVIDs, left ventricular internal dimensions at end‐systole. * P <0.05 between groups; ** P <0.01 between groups; *** P <0.005 between groups and **** P <0.001 between groups. AGK2 indicates a reversible inhibitor of SIRT2; Col, colchicine.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Colchicine Ameliorates Dilated Cardiomyopathy Via SIRT2 ‐Mediated Suppression of NLRP3 Inflammasome Activation

    doi: 10.1161/JAHA.122.025266

    Figure Lengend Snippet: A through C , Cardiac function is analyzed by 2‐dimensional murine echocardiography, left ventricular (LV) ejection fraction, LV fractional shortening, LV internal dimensions at end‐diastole, and LV internal dimensions at end‐systole values are measured at the end point of experiment (n=10 each group). D , Kaplan–Meier survival curve for each group mice followed for 4 weeks with or without doxorubicin challenge (n=25 each group). E , The changes of body weight from beginning to end (n=10 each group). F , Relative expression of ANP (atrial natriuretic peptide) mRNA and BNP (brain natriuretic peptide) mRNA are normalized to GAPDH mRNA in murine cardiac tissues at the end point of experiment. G and H , The representative hematoxylin and eosin staining ( G ) and Sirius red staining ( H ) of hearts in each group are shown. Quantification of interstitial fibrosis (% area) in hearts is shown on the right; n=8 each group. Five images per mouse are evaluated. Scale bar=50 μm. Data are shown as mean±SEM. Data of ( B , C , and E through G ) are analyzed by 1‐way ANOVA (Tukey post‐test). Data of ( D ) is analyzed by Mantel‐Cox test. ANP indicates atrial natriuretic peptide; BNP, brain natriuretic peptide; DCM, dilated cardiomyopathy; LVEF, left ventricular ejection fraction; LVFS, left ventricular fractional shortening; LVIDd, left ventricular internal dimensions at end‐diastole; and LVIDs, left ventricular internal dimensions at end‐systole. * P <0.05 between groups; ** P <0.01 between groups; *** P <0.005 between groups and **** P <0.001 between groups. AGK2 indicates a reversible inhibitor of SIRT2; Col, colchicine.

    Article Snippet: To identify the role of SIRT2, the SIRT2 inhibitor AGK2 (10 μmol/L, MCE, NJ, USA) was added to RPMI 1640 medium for 4 hours.

    Techniques: Expressing, Staining