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b type natriuretic peptide  (Elabscience Biotechnology)


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    Elabscience Biotechnology b type natriuretic peptide
    B Type Natriuretic Peptide, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 42 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    b type natriuretic peptide - by Bioz Stars, 2026-10
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    Article Title: Ginsenoside Rg1 Improves Cardiac Function and Ventricular Remodelling by Down-Regulating SH2B Adaptor Protein 1 Expression in Rats With Myocardial Infarction.
    Article Snippet: Objective: Acute myocardial infarction (AMI) remains the leading global cause of mortality.. This study explored the mechanism by which ginsenoside Rg1 (Rg1) ameliorates cardiac function and ventricular remodelling (VR) in rats with AMI by regulating SH2 domaincontaining adapter protein B1 (SH2B1).. Methods: An AMI rat model was established by ligating the left anterior descending coronary artery.

    Enzyme-linked Immunosorbent Assay:

    Article Title: Protective Effects of Pyrroloquinoline Quinone in Isoproterenol-Induced Myocardial Infarction in Rats
    Article Snippet: .. Serum troponin T (TNNT-2; BT Lab, Shanghai, China, Cat. No. E0306Ra) and B-type natriuretic peptide (BNP; Elabscience Biotechnology Co. Ltd., Wuhan, China, Cat. No. E-EL-R0126) levels were measured using competitive enzyme-linked immunosorbent assay (ELISA) kits according to the manufacturers’ instructions. ..

    Article Title: Shuxuening injection improves myocardial injury after myocardial infarction by regulating macrophage polarization via the TLR4/NF-κB and PI3K/Akt signaling pathways.
    Article Snippet: Background: Macrophage activation and polarization play pivotal roles in the inflammatory response and myocardial injury associated with myocardial infarction (MI).. Modulating macrophage polarization from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype is a promising therapeutic approach for MI.. Shuxuening injection (SXNI) is extensively utilized in clinical settings for MI treatment and has demonstrated therapeutic efficacy.



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    Empagliflozin regulates the multiorgan HFpEF phenotype in obese-diabetic mice. A Study protocol of empagliflozin treatment and assessment of multiorgan impairments, cardiac function, and cardiomyocyte excitation–contraction (EC) coupling. Empagliflozin (Empa) was administered in vivo for 4-wks in leptin receptor (Lepr)-deficient db/db mice with chronic aldosterone infusion ( db/db + Aldo) that induced heart failure with preserved ejection fraction (HFpEF) and in vehicle-treated wild-type mice (WT + Veh). B Blood glucose, body mass, <t>plasma</t> <t>B-type</t> <t>natriuretic</t> peptide <t>(BNP),</t> and pulmonary edema (quantified as wet-to-dry lung weight) in Empa-treated HFpEF mice. Kruskal–Wallis test with Dunn’s multiple comparison’s test. C Cardiac hypertrophy (quantified as heart weight to tibia length ratio, HW/TL), hepatomegaly, kidney weight, and sarcopenia (quantified as combined gastrocnemius and soleus muscle weights) in HFpEF. Welch ANOVA followed by Dunnett’s T3 multiple comparison’s test. The number of animals is shown in the figure
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    NRF-1 is negatively correlated with pyroptosis in HF patients. (a) Representative images of echocardiography in HF patients and NF controls. (b–g) Serum NT-proBNP, IL-18, IL-1β, NRF-1, GSDMD and caspase-1 level in HF patients (n = 15) and NF controls (n = 10). *P < 0.05, **P < 0.01, ***P < 0.001. GSDMD: gasdermin D; HF: heart failure; IL: interleukin; NF: normal cardiac function; NRF-1: nuclear respiratory factor-1; <t>NT-proBNP:</t> <t>N-terminal</t> <t>pro-B-type</t> <t>natriuretic</t> peptide.
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    NRF-1 is negatively correlated with pyroptosis in HF patients. (a) Representative images of echocardiography in HF patients and NF controls. (b–g) Serum NT-proBNP, IL-18, IL-1β, NRF-1, GSDMD and caspase-1 level in HF patients (n = 15) and NF controls (n = 10). *P < 0.05, **P < 0.01, ***P < 0.001. GSDMD: gasdermin D; HF: heart failure; IL: interleukin; NF: normal cardiac function; NRF-1: nuclear respiratory factor-1; <t>NT-proBNP:</t> <t>N-terminal</t> <t>pro-B-type</t> <t>natriuretic</t> peptide.
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    NRF-1 is negatively correlated with pyroptosis in HF patients. (a) Representative images of echocardiography in HF patients and NF controls. (b–g) Serum NT-proBNP, IL-18, IL-1β, NRF-1, GSDMD and caspase-1 level in HF patients (n = 15) and NF controls (n = 10). *P < 0.05, **P < 0.01, ***P < 0.001. GSDMD: gasdermin D; HF: heart failure; IL: interleukin; NF: normal cardiac function; NRF-1: nuclear respiratory factor-1; <t>NT-proBNP:</t> <t>N-terminal</t> <t>pro-B-type</t> <t>natriuretic</t> peptide.
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    NRF-1 is negatively correlated with pyroptosis in HF patients. (a) Representative images of echocardiography in HF patients and NF controls. (b–g) Serum NT-proBNP, IL-18, IL-1β, NRF-1, GSDMD and caspase-1 level in HF patients (n = 15) and NF controls (n = 10). *P < 0.05, **P < 0.01, ***P < 0.001. GSDMD: gasdermin D; HF: heart failure; IL: interleukin; NF: normal cardiac function; NRF-1: nuclear respiratory factor-1; <t>NT-proBNP:</t> <t>N-terminal</t> <t>pro-B-type</t> <t>natriuretic</t> peptide.
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    Right ventricular myocardium gene expression (A) and protein levels (B) , and circulating plasma mediator levels (C) in chronic thromboembolic pulmonary hypertension (CTEPH) and sham (sham). Gene expression data depicts genes involved in myofilament remodeling (MYH6 and MYH7, α- and β-myosin heavy chain isoforms, respectively), extracellular matrix fibrosis (COL1A1 and COL3A1, type I and III collagen chains, respectively), Ca 2+ -handling (ATP2A2, sarcoendoplasmic reticulum calcium ATPase 2; RYR2, cardiac ryanodine receptor), and neurohumoral mediators (NPPB, B-type natriuretic peptide; EDN1, endothelin-1; TNF, tumor necrosis factor-α). Data were averaged upon normalization for 2 internal control genes, GAPDH (glyceraldehyde-3-phosphate dehydrogenase) and RPL4 (ribosomal protein L4). Calcium-handling protein levels of sarcoendoplasmic reticulum Ca2+-ATPase 2a (SERCA2a) normalized for GAPDH and phospho-phospholamban (PLB) normalized for total PLB and representative Western blot bands are presented in (B) , whilst mediator plasma levels <t>of</t> <t>N-terminal</t> <t>pro–B-type</t> natriuretic peptide (NT-proBNP) and endothelin-1 (ET-1) are presented in panel C. In panels A and B data are presented relative to Sham reference levels (dashed lines). * P < 0.05 vs. Sham by Student's t -test or Mann–Whitney U -test, according to assumptions ( n = 6 and 7 in Sham and CTEPH, respectively).
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    Right ventricular myocardium gene expression (A) and protein levels (B) , and circulating plasma mediator levels (C) in chronic thromboembolic pulmonary hypertension (CTEPH) and sham (sham). Gene expression data depicts genes involved in myofilament remodeling (MYH6 and MYH7, α- and β-myosin heavy chain isoforms, respectively), extracellular matrix fibrosis (COL1A1 and COL3A1, type I and III collagen chains, respectively), Ca 2+ -handling (ATP2A2, sarcoendoplasmic reticulum calcium ATPase 2; RYR2, cardiac ryanodine receptor), and neurohumoral mediators (NPPB, B-type natriuretic peptide; EDN1, endothelin-1; TNF, tumor necrosis factor-α). Data were averaged upon normalization for 2 internal control genes, GAPDH (glyceraldehyde-3-phosphate dehydrogenase) and RPL4 (ribosomal protein L4). Calcium-handling protein levels of sarcoendoplasmic reticulum Ca2+-ATPase 2a (SERCA2a) normalized for GAPDH and phospho-phospholamban (PLB) normalized for total PLB and representative Western blot bands are presented in (B) , whilst mediator plasma levels <t>of</t> <t>N-terminal</t> <t>pro–B-type</t> natriuretic peptide (NT-proBNP) and endothelin-1 (ET-1) are presented in panel C. In panels A and B data are presented relative to Sham reference levels (dashed lines). * P < 0.05 vs. Sham by Student's t -test or Mann–Whitney U -test, according to assumptions ( n = 6 and 7 in Sham and CTEPH, respectively).
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    Right ventricular myocardium gene expression (A) and protein levels (B) , and circulating plasma mediator levels (C) in chronic thromboembolic pulmonary hypertension (CTEPH) and sham (sham). Gene expression data depicts genes involved in myofilament remodeling (MYH6 and MYH7, α- and β-myosin heavy chain isoforms, respectively), extracellular matrix fibrosis (COL1A1 and COL3A1, type I and III collagen chains, respectively), Ca 2+ -handling (ATP2A2, sarcoendoplasmic reticulum calcium ATPase 2; RYR2, cardiac ryanodine receptor), and neurohumoral mediators (NPPB, B-type natriuretic peptide; EDN1, endothelin-1; TNF, tumor necrosis factor-α). Data were averaged upon normalization for 2 internal control genes, GAPDH (glyceraldehyde-3-phosphate dehydrogenase) and RPL4 (ribosomal protein L4). Calcium-handling protein levels of sarcoendoplasmic reticulum Ca2+-ATPase 2a (SERCA2a) normalized for GAPDH and phospho-phospholamban (PLB) normalized for total PLB and representative Western blot bands are presented in (B) , whilst mediator plasma levels <t>of</t> <t>N-terminal</t> <t>pro–B-type</t> natriuretic peptide (NT-proBNP) and endothelin-1 (ET-1) are presented in panel C. In panels A and B data are presented relative to Sham reference levels (dashed lines). * P < 0.05 vs. Sham by Student's t -test or Mann–Whitney U -test, according to assumptions ( n = 6 and 7 in Sham and CTEPH, respectively).
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    Image Search Results


    Empagliflozin regulates the multiorgan HFpEF phenotype in obese-diabetic mice. A Study protocol of empagliflozin treatment and assessment of multiorgan impairments, cardiac function, and cardiomyocyte excitation–contraction (EC) coupling. Empagliflozin (Empa) was administered in vivo for 4-wks in leptin receptor (Lepr)-deficient db/db mice with chronic aldosterone infusion ( db/db + Aldo) that induced heart failure with preserved ejection fraction (HFpEF) and in vehicle-treated wild-type mice (WT + Veh). B Blood glucose, body mass, plasma B-type natriuretic peptide (BNP), and pulmonary edema (quantified as wet-to-dry lung weight) in Empa-treated HFpEF mice. Kruskal–Wallis test with Dunn’s multiple comparison’s test. C Cardiac hypertrophy (quantified as heart weight to tibia length ratio, HW/TL), hepatomegaly, kidney weight, and sarcopenia (quantified as combined gastrocnemius and soleus muscle weights) in HFpEF. Welch ANOVA followed by Dunnett’s T3 multiple comparison’s test. The number of animals is shown in the figure

    Journal: Basic Research in Cardiology

    Article Title: Empagliflozin restores cardiac function in obese-diabetic HFpEF mice but further alters gene expression

    doi: 10.1007/s00395-026-01184-7

    Figure Lengend Snippet: Empagliflozin regulates the multiorgan HFpEF phenotype in obese-diabetic mice. A Study protocol of empagliflozin treatment and assessment of multiorgan impairments, cardiac function, and cardiomyocyte excitation–contraction (EC) coupling. Empagliflozin (Empa) was administered in vivo for 4-wks in leptin receptor (Lepr)-deficient db/db mice with chronic aldosterone infusion ( db/db + Aldo) that induced heart failure with preserved ejection fraction (HFpEF) and in vehicle-treated wild-type mice (WT + Veh). B Blood glucose, body mass, plasma B-type natriuretic peptide (BNP), and pulmonary edema (quantified as wet-to-dry lung weight) in Empa-treated HFpEF mice. Kruskal–Wallis test with Dunn’s multiple comparison’s test. C Cardiac hypertrophy (quantified as heart weight to tibia length ratio, HW/TL), hepatomegaly, kidney weight, and sarcopenia (quantified as combined gastrocnemius and soleus muscle weights) in HFpEF. Welch ANOVA followed by Dunnett’s T3 multiple comparison’s test. The number of animals is shown in the figure

    Article Snippet: B-type natriuretic peptide (BNP) levels were measured in blood plasma by ELISA (RayBiotech, EIAM-BNP-1).

    Techniques: In Vivo, Clinical Proteomics

    NRF-1 is negatively correlated with pyroptosis in HF patients. (a) Representative images of echocardiography in HF patients and NF controls. (b–g) Serum NT-proBNP, IL-18, IL-1β, NRF-1, GSDMD and caspase-1 level in HF patients (n = 15) and NF controls (n = 10). *P < 0.05, **P < 0.01, ***P < 0.001. GSDMD: gasdermin D; HF: heart failure; IL: interleukin; NF: normal cardiac function; NRF-1: nuclear respiratory factor-1; NT-proBNP: N-terminal pro-B-type natriuretic peptide.

    Journal: Cardiology Research

    Article Title: Nuclear Respiratory Factor-1 Ameliorates Heart Failure by Suppressing Cardiomyocyte Pyroptosis-Associated Signaling Via the Downregulation of Gasdermin D and Caspase-1

    doi: 10.14740/cr2153

    Figure Lengend Snippet: NRF-1 is negatively correlated with pyroptosis in HF patients. (a) Representative images of echocardiography in HF patients and NF controls. (b–g) Serum NT-proBNP, IL-18, IL-1β, NRF-1, GSDMD and caspase-1 level in HF patients (n = 15) and NF controls (n = 10). *P < 0.05, **P < 0.01, ***P < 0.001. GSDMD: gasdermin D; HF: heart failure; IL: interleukin; NF: normal cardiac function; NRF-1: nuclear respiratory factor-1; NT-proBNP: N-terminal pro-B-type natriuretic peptide.

    Article Snippet: ELISA kits were used to detect N-terminal pro-B-type natriuretic peptide (NT-proBNP, EK1393, Multi Science, Hangzhou, China), NRF-1 (E15022h, EIAab, Wuhan, China), IL-18 (EK118S, Multi Science, Hangzhou, China), IL-1β (EK101B, Multi Science, Hangzhou, China), gasdermin D (GSDMD) (E15480h, EIAab, Wuhan, China), and caspase-1 (E1592h, EIAab, Wuhan, China), following the instructions of manufacturers.

    Techniques:

    Right ventricular myocardium gene expression (A) and protein levels (B) , and circulating plasma mediator levels (C) in chronic thromboembolic pulmonary hypertension (CTEPH) and sham (sham). Gene expression data depicts genes involved in myofilament remodeling (MYH6 and MYH7, α- and β-myosin heavy chain isoforms, respectively), extracellular matrix fibrosis (COL1A1 and COL3A1, type I and III collagen chains, respectively), Ca 2+ -handling (ATP2A2, sarcoendoplasmic reticulum calcium ATPase 2; RYR2, cardiac ryanodine receptor), and neurohumoral mediators (NPPB, B-type natriuretic peptide; EDN1, endothelin-1; TNF, tumor necrosis factor-α). Data were averaged upon normalization for 2 internal control genes, GAPDH (glyceraldehyde-3-phosphate dehydrogenase) and RPL4 (ribosomal protein L4). Calcium-handling protein levels of sarcoendoplasmic reticulum Ca2+-ATPase 2a (SERCA2a) normalized for GAPDH and phospho-phospholamban (PLB) normalized for total PLB and representative Western blot bands are presented in (B) , whilst mediator plasma levels of N-terminal pro–B-type natriuretic peptide (NT-proBNP) and endothelin-1 (ET-1) are presented in panel C. In panels A and B data are presented relative to Sham reference levels (dashed lines). * P < 0.05 vs. Sham by Student's t -test or Mann–Whitney U -test, according to assumptions ( n = 6 and 7 in Sham and CTEPH, respectively).

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: A swine model of severe chronic thromboembolic pulmonary hypertension induced by repeated pulmonary artery long suture injection

    doi: 10.3389/fcvm.2025.1736958

    Figure Lengend Snippet: Right ventricular myocardium gene expression (A) and protein levels (B) , and circulating plasma mediator levels (C) in chronic thromboembolic pulmonary hypertension (CTEPH) and sham (sham). Gene expression data depicts genes involved in myofilament remodeling (MYH6 and MYH7, α- and β-myosin heavy chain isoforms, respectively), extracellular matrix fibrosis (COL1A1 and COL3A1, type I and III collagen chains, respectively), Ca 2+ -handling (ATP2A2, sarcoendoplasmic reticulum calcium ATPase 2; RYR2, cardiac ryanodine receptor), and neurohumoral mediators (NPPB, B-type natriuretic peptide; EDN1, endothelin-1; TNF, tumor necrosis factor-α). Data were averaged upon normalization for 2 internal control genes, GAPDH (glyceraldehyde-3-phosphate dehydrogenase) and RPL4 (ribosomal protein L4). Calcium-handling protein levels of sarcoendoplasmic reticulum Ca2+-ATPase 2a (SERCA2a) normalized for GAPDH and phospho-phospholamban (PLB) normalized for total PLB and representative Western blot bands are presented in (B) , whilst mediator plasma levels of N-terminal pro–B-type natriuretic peptide (NT-proBNP) and endothelin-1 (ET-1) are presented in panel C. In panels A and B data are presented relative to Sham reference levels (dashed lines). * P < 0.05 vs. Sham by Student's t -test or Mann–Whitney U -test, according to assumptions ( n = 6 and 7 in Sham and CTEPH, respectively).

    Article Snippet: Previously aliquoted plasma samples were thawed on ice and assayed for N-terminal pro–B-type natriuretic peptide (NT-proBNP; CSB-EQ027465PI, Cusabio) and endothelin-1 (ET-1; ADI-900-020A, Enzo Life Sciences Inc) in duplicate according to the manufacturer's instructions.

    Techniques: Gene Expression, Clinical Proteomics, Control, Western Blot, MANN-WHITNEY