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Hopeaphenol alleviates Ang II-induced cardiomyocyte hypertrophy Via AMPK/SIRT1 activation. ( A , B ) CCK-8 assay for non-toxic ranges of hopeaphenol (0–50 μM) and the AMPK inhibitor CC (0–50 μM) (24 h). ( C ) Cells modeling flowchart. ( D – G ) Western blot analysis of p-AMPK/AMPK ( E ), SIRT1 ( F ) and BNP ( G ) in HL-1 cells with densitometric analysis. ( H – K ) Immunofluorescence of p-AMPK ( H ) and SIRT1 ( J ) with DAPI (blue) (scale bar, 25 μm); quantification of fluorescence intensity ( I , K ). ( L – M ) Phalloidin staining (green) of F-actin with DAPI (blue) ( L ) and quantification of cell cross-sectional area ( M ) (scale bar, 25 μm). Cells were pretreated with HP (1, 5, 10 μM) for 2 h or CC (10 μM) for 1 h, followed by stimulation with <t>Ang</t> <t>II</t> (1 μM) for 24 h. Exact p -values for all post hoc comparisons are indicated on the graphs. Data are presented as mean ± SEM ( n = 6). ns, not significant; HP, Hopeaphenol.
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Hopeaphenol alleviates Ang II-induced cardiomyocyte hypertrophy Via AMPK/SIRT1 activation. ( A , B ) CCK-8 assay for non-toxic ranges of hopeaphenol (0–50 μM) and the AMPK inhibitor CC (0–50 μM) (24 h). ( C ) Cells modeling flowchart. ( D – G ) Western blot analysis of p-AMPK/AMPK ( E ), SIRT1 ( F ) and BNP ( G ) in HL-1 cells with densitometric analysis. ( H – K ) Immunofluorescence of p-AMPK ( H ) and SIRT1 ( J ) with DAPI (blue) (scale bar, 25 μm); quantification of fluorescence intensity ( I , K ). ( L – M ) Phalloidin staining (green) of F-actin with DAPI (blue) ( L ) and quantification of cell cross-sectional area ( M ) (scale bar, 25 μm). Cells were pretreated with HP (1, 5, 10 μM) for 2 h or CC (10 μM) for 1 h, followed by stimulation with Ang II (1 μM) for 24 h. Exact p -values for all post hoc comparisons are indicated on the graphs. Data are presented as mean ± SEM ( n = 6). ns, not significant; HP, Hopeaphenol.

Journal: Nutrients

Article Title: Unlocking Hopeaphenol: A Potent Ally Against Cardiac Hypertrophy via AMPK Activation

doi: 10.3390/nu17183025

Figure Lengend Snippet: Hopeaphenol alleviates Ang II-induced cardiomyocyte hypertrophy Via AMPK/SIRT1 activation. ( A , B ) CCK-8 assay for non-toxic ranges of hopeaphenol (0–50 μM) and the AMPK inhibitor CC (0–50 μM) (24 h). ( C ) Cells modeling flowchart. ( D – G ) Western blot analysis of p-AMPK/AMPK ( E ), SIRT1 ( F ) and BNP ( G ) in HL-1 cells with densitometric analysis. ( H – K ) Immunofluorescence of p-AMPK ( H ) and SIRT1 ( J ) with DAPI (blue) (scale bar, 25 μm); quantification of fluorescence intensity ( I , K ). ( L – M ) Phalloidin staining (green) of F-actin with DAPI (blue) ( L ) and quantification of cell cross-sectional area ( M ) (scale bar, 25 μm). Cells were pretreated with HP (1, 5, 10 μM) for 2 h or CC (10 μM) for 1 h, followed by stimulation with Ang II (1 μM) for 24 h. Exact p -values for all post hoc comparisons are indicated on the graphs. Data are presented as mean ± SEM ( n = 6). ns, not significant; HP, Hopeaphenol.

Article Snippet: Compound C (#S7840) and Angiotensin II (Ang II, #HY-P0108) were obtained from Selleck Chemicals (Houston, TX, USA) and MedChemExpress (MCE, Monmouth Jct., NJ, USA), respectively.

Techniques: Activation Assay, CCK-8 Assay, Western Blot, Immunofluorescence, Fluorescence, Staining

Hopeaphenol reduces mitochondrial ROS and enhances membrane potential in Ang II-treated HL-1 cardiomyocytes. ( A , B ) Mitochondrial ROS detection (DCFH-DA, green) ( A ) and quantification of fluorescence intensity ( B ) (scale bar = 25 μm). ( C , D ) JC-1 staining (red: J-aggregates, green: J-monomers) ( C ) and red/green fluorescence ratio (ΔΨm) ( D ) (scale bar = 25 μm). Cells were pretreated as in . Exact p -values for all post hoc comparisons are indicated on the graphs. Data are presented as mean ± SEM ( n = 6). ns, not significant; HP, Hopeaphenol.

Journal: Nutrients

Article Title: Unlocking Hopeaphenol: A Potent Ally Against Cardiac Hypertrophy via AMPK Activation

doi: 10.3390/nu17183025

Figure Lengend Snippet: Hopeaphenol reduces mitochondrial ROS and enhances membrane potential in Ang II-treated HL-1 cardiomyocytes. ( A , B ) Mitochondrial ROS detection (DCFH-DA, green) ( A ) and quantification of fluorescence intensity ( B ) (scale bar = 25 μm). ( C , D ) JC-1 staining (red: J-aggregates, green: J-monomers) ( C ) and red/green fluorescence ratio (ΔΨm) ( D ) (scale bar = 25 μm). Cells were pretreated as in . Exact p -values for all post hoc comparisons are indicated on the graphs. Data are presented as mean ± SEM ( n = 6). ns, not significant; HP, Hopeaphenol.

Article Snippet: Compound C (#S7840) and Angiotensin II (Ang II, #HY-P0108) were obtained from Selleck Chemicals (Houston, TX, USA) and MedChemExpress (MCE, Monmouth Jct., NJ, USA), respectively.

Techniques: Membrane, Fluorescence, Staining

AMPK inhibition by Compound C abolishes Hopeaphenol-mediated protection against Ang II-induced hypertrophy and apoptosis in HL-1 cardiomyocytes. ( A – E ) Western blot analysis of PGC-1α, SIRT1, β-MHC, and BNP ( A ) and their quantification (( B – E ), normalized to β-actin). ( F – H ) qPCR analysis of SIRT1, BNP, and β-MHC mRNA. ( I – K ) Western blot analysis of Bax, Bcl-2, and cleaved caspase-3 ( I ), and quantification of the Bax/Bcl-2 ratio ( J ) and cleaved caspase-3 ( K ). Cells were pretreated as in . Exact p values for all post hoc comparisons are indicated on the graphs. Data are presented as mean ± SEM ( n = 3 for panels ( I – K ); n = 6 for others). ns, not significant; c-Casp3, cleaved caspase-3; HP, Hopeaphenol.

Journal: Nutrients

Article Title: Unlocking Hopeaphenol: A Potent Ally Against Cardiac Hypertrophy via AMPK Activation

doi: 10.3390/nu17183025

Figure Lengend Snippet: AMPK inhibition by Compound C abolishes Hopeaphenol-mediated protection against Ang II-induced hypertrophy and apoptosis in HL-1 cardiomyocytes. ( A – E ) Western blot analysis of PGC-1α, SIRT1, β-MHC, and BNP ( A ) and their quantification (( B – E ), normalized to β-actin). ( F – H ) qPCR analysis of SIRT1, BNP, and β-MHC mRNA. ( I – K ) Western blot analysis of Bax, Bcl-2, and cleaved caspase-3 ( I ), and quantification of the Bax/Bcl-2 ratio ( J ) and cleaved caspase-3 ( K ). Cells were pretreated as in . Exact p values for all post hoc comparisons are indicated on the graphs. Data are presented as mean ± SEM ( n = 3 for panels ( I – K ); n = 6 for others). ns, not significant; c-Casp3, cleaved caspase-3; HP, Hopeaphenol.

Article Snippet: Compound C (#S7840) and Angiotensin II (Ang II, #HY-P0108) were obtained from Selleck Chemicals (Houston, TX, USA) and MedChemExpress (MCE, Monmouth Jct., NJ, USA), respectively.

Techniques: Inhibition, Western Blot

Schematic of hopeaphenol alleviating cardiac hypertrophy. The left panel shows the Ang II/TAC-induced pathological process (HL-1 cells, C57 mice), characterized by mitochondrial dysfunction, cardiomyocyte hypertrophy, and fibrosis. The right panel depicts that Hopeaphenol primarily activates the AMPK/SIRT1 signaling pathway to improve cardiac and mitochondrial function, and to inhibit hypertrophy, fibrosis, and apoptosis; notably, due to the potential off-target effects of CC (Compound C), the involvement of other pathways in these processes cannot be completely ruled out. Meanwhile, CC (Compound C) blocks the activity of AMPK, which in turn abrogates the aforementioned beneficial effects of Hopeaphenol—this observation strongly supports the role of AMPK in mediating Hopeaphenol’s cardioprotection (by Figdraw). CC, Compound C.

Journal: Nutrients

Article Title: Unlocking Hopeaphenol: A Potent Ally Against Cardiac Hypertrophy via AMPK Activation

doi: 10.3390/nu17183025

Figure Lengend Snippet: Schematic of hopeaphenol alleviating cardiac hypertrophy. The left panel shows the Ang II/TAC-induced pathological process (HL-1 cells, C57 mice), characterized by mitochondrial dysfunction, cardiomyocyte hypertrophy, and fibrosis. The right panel depicts that Hopeaphenol primarily activates the AMPK/SIRT1 signaling pathway to improve cardiac and mitochondrial function, and to inhibit hypertrophy, fibrosis, and apoptosis; notably, due to the potential off-target effects of CC (Compound C), the involvement of other pathways in these processes cannot be completely ruled out. Meanwhile, CC (Compound C) blocks the activity of AMPK, which in turn abrogates the aforementioned beneficial effects of Hopeaphenol—this observation strongly supports the role of AMPK in mediating Hopeaphenol’s cardioprotection (by Figdraw). CC, Compound C.

Article Snippet: Compound C (#S7840) and Angiotensin II (Ang II, #HY-P0108) were obtained from Selleck Chemicals (Houston, TX, USA) and MedChemExpress (MCE, Monmouth Jct., NJ, USA), respectively.

Techniques: Activity Assay