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cells  (MedChemExpress)


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    MedChemExpress cells
    Cells, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-n0770/Isoliensinine/pmc12299100-144-4-23
    Average 93 stars, based on 5 article reviews
    cells - by Bioz Stars, 2026-10
    93/100 stars

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    Functional Assay:

    Article Title: Isoliensinine Ameliorates Pathological Cardiac Hypertrophy After Aerobic Exercise by Activating Cytochrome c Oxidase Subunit 6A2
    Article Snippet: .. 3) To validate the functional role of isoliensinine (ILS), exogenous ILS (HY-N0770, MCE, USA) was administered to assess its effects on cardiac structure and function in TAC mice. ..



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    (A) CCK-8 assay assessing cytotoxicity <t>of</t> <t>isoliensinine</t> <t>(ILS).</t> Cell viability remained unaffected at 5 μM ILS, confirming its non-toxic concentration for subsequent experiments. (B-D) qPCR analysis of hypertrophic markers: ANP, BNP, and β-MHC. mRNA levels were normalized to β-actin. (E-F) Phalloidin staining (red: F-actin; blue: nuclei) and quantitative analysis of cell surface area. (G-I) Fluorescence imaging and quantification of intracellular ROS (DHE probe, red fluorescence) and mitochondrial superoxide (MitoSOX Green probe, green fluorescence). (J-M) Western blot analysis of apoptosis-related proteins: Caspase3, Bax, Bcl-2, and β-actin (loading control). Data presented as mean ± SEM (n ≥ 3), *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.
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    (A) CCK-8 assay assessing cytotoxicity <t>of</t> <t>isoliensinine</t> <t>(ILS).</t> Cell viability remained unaffected at 5 μM ILS, confirming its non-toxic concentration for subsequent experiments. (B-D) qPCR analysis of hypertrophic markers: ANP, BNP, and β-MHC. mRNA levels were normalized to β-actin. (E-F) Phalloidin staining (red: F-actin; blue: nuclei) and quantitative analysis of cell surface area. (G-I) Fluorescence imaging and quantification of intracellular ROS (DHE probe, red fluorescence) and mitochondrial superoxide (MitoSOX Green probe, green fluorescence). (J-M) Western blot analysis of apoptosis-related proteins: Caspase3, Bax, Bcl-2, and β-actin (loading control). Data presented as mean ± SEM (n ≥ 3), *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.
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    Metabolomic profiling of cardiac tissues: (A) Heatmap of differentially expressed metabolites between Swim and control groups; (B) Volcano plot highlighting <t>isoliensinine</t> (red dot) as a key upregulated metabolite in the Swim group (log2 fold change >1.5, p < 0.05). (C) Chemical structure of isoliensinine, a bioactive alkaloid derived from Nelumbo nucifera. Echocardiographic assessment of cardiac function: (D) Representative images of left ventricular morphology; (E) Heart rate; (F) Ejection fraction (EF); (G) fractional shortening (FS); (H-I) Left ventricular end-diastolic diameter (LVIDd) and end-systolic diameter (LVIDs). Data presented as mean ± SEM (n = 10/group). P < 0.05 was considered to indicate a statistically significant difference. (J-K) Heart weight-to-body weight ratio (HW/BW) and heart weight-to-tibia length ratio (HW/TL). Isoliensinine significantly attenuated TAC-induced cardiac hypertrophy. (L-M) Serum levels of ANP and BNP measured by ELISA. (N) qPCR analysis of hypertrophy markers (ANP, BNP, β-MHC). mRNA levels were normalized to β-actin. Data presented as mean ± SEM (n = 6), *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.
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    cells  (MedChemExpress)
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    Metabolomic profiling of cardiac tissues: (A) Heatmap of differentially expressed metabolites between Swim and control groups; (B) Volcano plot highlighting <t>isoliensinine</t> (red dot) as a key upregulated metabolite in the Swim group (log2 fold change >1.5, p < 0.05). (C) Chemical structure of isoliensinine, a bioactive alkaloid derived from Nelumbo nucifera. Echocardiographic assessment of cardiac function: (D) Representative images of left ventricular morphology; (E) Heart rate; (F) Ejection fraction (EF); (G) fractional shortening (FS); (H-I) Left ventricular end-diastolic diameter (LVIDd) and end-systolic diameter (LVIDs). Data presented as mean ± SEM (n = 10/group). P < 0.05 was considered to indicate a statistically significant difference. (J-K) Heart weight-to-body weight ratio (HW/BW) and heart weight-to-tibia length ratio (HW/TL). Isoliensinine significantly attenuated TAC-induced cardiac hypertrophy. (L-M) Serum levels of ANP and BNP measured by ELISA. (N) qPCR analysis of hypertrophy markers (ANP, BNP, β-MHC). mRNA levels were normalized to β-actin. Data presented as mean ± SEM (n = 6), *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.
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    (A) CCK-8 assay assessing cytotoxicity of isoliensinine (ILS). Cell viability remained unaffected at 5 μM ILS, confirming its non-toxic concentration for subsequent experiments. (B-D) qPCR analysis of hypertrophic markers: ANP, BNP, and β-MHC. mRNA levels were normalized to β-actin. (E-F) Phalloidin staining (red: F-actin; blue: nuclei) and quantitative analysis of cell surface area. (G-I) Fluorescence imaging and quantification of intracellular ROS (DHE probe, red fluorescence) and mitochondrial superoxide (MitoSOX Green probe, green fluorescence). (J-M) Western blot analysis of apoptosis-related proteins: Caspase3, Bax, Bcl-2, and β-actin (loading control). Data presented as mean ± SEM (n ≥ 3), *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

    Journal: bioRxiv

    Article Title: Isoliensinine Ameliorates Pathological Cardiac Hypertrophy After Aerobic Exercise by Activating Cytochrome c Oxidase Subunit 6A2

    doi: 10.1101/2025.07.07.663610

    Figure Lengend Snippet: (A) CCK-8 assay assessing cytotoxicity of isoliensinine (ILS). Cell viability remained unaffected at 5 μM ILS, confirming its non-toxic concentration for subsequent experiments. (B-D) qPCR analysis of hypertrophic markers: ANP, BNP, and β-MHC. mRNA levels were normalized to β-actin. (E-F) Phalloidin staining (red: F-actin; blue: nuclei) and quantitative analysis of cell surface area. (G-I) Fluorescence imaging and quantification of intracellular ROS (DHE probe, red fluorescence) and mitochondrial superoxide (MitoSOX Green probe, green fluorescence). (J-M) Western blot analysis of apoptosis-related proteins: Caspase3, Bax, Bcl-2, and β-actin (loading control). Data presented as mean ± SEM (n ≥ 3), *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

    Article Snippet: 3) To validate the functional role of isoliensinine (ILS), exogenous ILS (HY-N0770, MCE, USA) was administered to assess its effects on cardiac structure and function in TAC mice.

    Techniques: CCK-8 Assay, Concentration Assay, Staining, Fluorescence, Imaging, Western Blot, Control

    Metabolomic profiling of cardiac tissues: (A) Heatmap of differentially expressed metabolites between Swim and control groups; (B) Volcano plot highlighting isoliensinine (red dot) as a key upregulated metabolite in the Swim group (log2 fold change >1.5, p < 0.05). (C) Chemical structure of isoliensinine, a bioactive alkaloid derived from Nelumbo nucifera. Echocardiographic assessment of cardiac function: (D) Representative images of left ventricular morphology; (E) Heart rate; (F) Ejection fraction (EF); (G) fractional shortening (FS); (H-I) Left ventricular end-diastolic diameter (LVIDd) and end-systolic diameter (LVIDs). Data presented as mean ± SEM (n = 10/group). P < 0.05 was considered to indicate a statistically significant difference. (J-K) Heart weight-to-body weight ratio (HW/BW) and heart weight-to-tibia length ratio (HW/TL). Isoliensinine significantly attenuated TAC-induced cardiac hypertrophy. (L-M) Serum levels of ANP and BNP measured by ELISA. (N) qPCR analysis of hypertrophy markers (ANP, BNP, β-MHC). mRNA levels were normalized to β-actin. Data presented as mean ± SEM (n = 6), *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

    Journal: bioRxiv

    Article Title: Isoliensinine Ameliorates Pathological Cardiac Hypertrophy After Aerobic Exercise by Activating Cytochrome c Oxidase Subunit 6A2

    doi: 10.1101/2025.07.07.663610

    Figure Lengend Snippet: Metabolomic profiling of cardiac tissues: (A) Heatmap of differentially expressed metabolites between Swim and control groups; (B) Volcano plot highlighting isoliensinine (red dot) as a key upregulated metabolite in the Swim group (log2 fold change >1.5, p < 0.05). (C) Chemical structure of isoliensinine, a bioactive alkaloid derived from Nelumbo nucifera. Echocardiographic assessment of cardiac function: (D) Representative images of left ventricular morphology; (E) Heart rate; (F) Ejection fraction (EF); (G) fractional shortening (FS); (H-I) Left ventricular end-diastolic diameter (LVIDd) and end-systolic diameter (LVIDs). Data presented as mean ± SEM (n = 10/group). P < 0.05 was considered to indicate a statistically significant difference. (J-K) Heart weight-to-body weight ratio (HW/BW) and heart weight-to-tibia length ratio (HW/TL). Isoliensinine significantly attenuated TAC-induced cardiac hypertrophy. (L-M) Serum levels of ANP and BNP measured by ELISA. (N) qPCR analysis of hypertrophy markers (ANP, BNP, β-MHC). mRNA levels were normalized to β-actin. Data presented as mean ± SEM (n = 6), *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

    Article Snippet: 3) To validate the functional role of isoliensinine (ILS), exogenous ILS (HY-N0770, MCE, USA) was administered to assess its effects on cardiac structure and function in TAC mice.

    Techniques: Metabolomic, Control, Derivative Assay, Enzyme-linked Immunosorbent Assay

    (A) CCK-8 assay assessing cytotoxicity of isoliensinine (ILS). Cell viability remained unaffected at 5 μM ILS, confirming its non-toxic concentration for subsequent experiments. (B-D) qPCR analysis of hypertrophic markers: ANP, BNP, and β-MHC. mRNA levels were normalized to β-actin. (E-F) Phalloidin staining (red: F-actin; blue: nuclei) and quantitative analysis of cell surface area. (G-I) Fluorescence imaging and quantification of intracellular ROS (DHE probe, red fluorescence) and mitochondrial superoxide (MitoSOX Green probe, green fluorescence). (J-M) Western blot analysis of apoptosis-related proteins: Caspase3, Bax, Bcl-2, and β-actin (loading control). Data presented as mean ± SEM (n ≥ 3), *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

    Journal: bioRxiv

    Article Title: Isoliensinine Ameliorates Pathological Cardiac Hypertrophy After Aerobic Exercise by Activating Cytochrome c Oxidase Subunit 6A2

    doi: 10.1101/2025.07.07.663610

    Figure Lengend Snippet: (A) CCK-8 assay assessing cytotoxicity of isoliensinine (ILS). Cell viability remained unaffected at 5 μM ILS, confirming its non-toxic concentration for subsequent experiments. (B-D) qPCR analysis of hypertrophic markers: ANP, BNP, and β-MHC. mRNA levels were normalized to β-actin. (E-F) Phalloidin staining (red: F-actin; blue: nuclei) and quantitative analysis of cell surface area. (G-I) Fluorescence imaging and quantification of intracellular ROS (DHE probe, red fluorescence) and mitochondrial superoxide (MitoSOX Green probe, green fluorescence). (J-M) Western blot analysis of apoptosis-related proteins: Caspase3, Bax, Bcl-2, and β-actin (loading control). Data presented as mean ± SEM (n ≥ 3), *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

    Article Snippet: 3) To validate the functional role of isoliensinine (ILS), exogenous ILS (HY-N0770, MCE, USA) was administered to assess its effects on cardiac structure and function in TAC mice.

    Techniques: CCK-8 Assay, Concentration Assay, Staining, Fluorescence, Imaging, Western Blot, Control