mouse nt probnp elisa kit  (Novus Biologicals)

Journal: Frontiers in Immunology

Article Title: SLC31A1 knockdown mitigates post-MI heart failure via regulation of copper metabolism

doi: 10.3389/fimmu.2026.1707203

Figure Lengend Snippet: SLC31A1 is abundantly expressed in post-AMI HF mouse models, silencing of which mitigates post-AMI HF by inhibiting cardiomyocyte apoptosis. (A, B) LVEF and LVEDP detected by echocardiography, n = 12; (C) The serum NT-proBNP level measured by ELISA, n = 12; (D) Representative images of TTC-stained heart sections and quantification of myocardial infarction, n = 6; (E) Cardiomyocyte apoptosis assessed by TUNEL staining, n = 6; (F) Sorting of macrophages (F4/80 + /CD11b + ) by flow cytometry; (G) mRNA expression of SLC31A1 determined by RT-qPCR, n = 12; (H) The level of SLC31A1 protein determined by western blot, n = 3. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Levels of N-terminal pro-brain natriuretic peptide (NT-proBNP), IL-1β, tumor necrosis factor-α (TNF-α) and HMGB1 were measured in the mouse serum and cell supernatants using ELISA kits (Elabscience) (NT-proBNP kit: E-EL-M0834; IL-1β kit: E-EL-M0037; TNF-α kit: E-EL-M3063; HMGB1 kit: E-EL-M0676).

Techniques: Enzyme-linked Immunosorbent Assay, Staining, TUNEL Assay, Flow Cytometry, Expressing, Quantitative RT-PCR, Western Blot, Standard Deviation

Journal: Frontiers in Immunology

Article Title: SLC31A1 knockdown mitigates post-MI heart failure via regulation of copper metabolism

doi: 10.3389/fimmu.2026.1707203

Figure Lengend Snippet: SLC31A1 knockdown arrests cuproptosis and HMGB1 release by regulating copper metabolism imbalance, alleviating inflammatory responses in macrophages of mice with HF after AMI. (A-C) Cu 2+ level, ATP content and SDH activity in mouse macrophages determined by kits; (D) Levels of cuproptosis-related proteins FDX1 and DLAT in mouse macrophages measured by western blot; (E) Mitochondrial damage in cells detected by TEM; Levels of HMGB1 (F) , IL-1β (G) , and TNF-α (H) in mouse serum measured by ELISA. n = 12. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Levels of N-terminal pro-brain natriuretic peptide (NT-proBNP), IL-1β, tumor necrosis factor-α (TNF-α) and HMGB1 were measured in the mouse serum and cell supernatants using ELISA kits (Elabscience) (NT-proBNP kit: E-EL-M0834; IL-1β kit: E-EL-M0037; TNF-α kit: E-EL-M3063; HMGB1 kit: E-EL-M0676).

Techniques: Knockdown, Activity Assay, Western Blot, Enzyme-linked Immunosorbent Assay, Standard Deviation

Journal: Frontiers in Immunology

Article Title: SLC31A1 knockdown mitigates post-MI heart failure via regulation of copper metabolism

doi: 10.3389/fimmu.2026.1707203

Figure Lengend Snippet: ATTM inhibits cuproptosis in macrophages, impedes cardiomyocyte apoptosis and relieves HF after AMI in mice. (A-C) Cu 2+ level, ATP content, and SDH activity in mouse macrophages determined by kits, n = 12; (D) Levels of cuproptosis-related proteins FDX1 and DLAT in mouse macrophages measured by western blot, n = 12; (E) Mitochondrial damage in cells assessed by TEM; Levels of HMGB1 (F) , IL-1β (G) , and TNF-α (H) in mouse serum measured by ELISA, n = 12; LVEF (I) and LVEDP (J) detected by echocardiography, n = 12; K, The NT-proBNP level in mouse serum measured by ELISA, n = 12; L, Representative images of TTC-stained heart sections and quantification of myocardial infarction, n = 6; M, Cardiomyocyte apoptosis assessed by TUNEL staining, n = 6. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Levels of N-terminal pro-brain natriuretic peptide (NT-proBNP), IL-1β, tumor necrosis factor-α (TNF-α) and HMGB1 were measured in the mouse serum and cell supernatants using ELISA kits (Elabscience) (NT-proBNP kit: E-EL-M0834; IL-1β kit: E-EL-M0037; TNF-α kit: E-EL-M3063; HMGB1 kit: E-EL-M0676).

Techniques: Activity Assay, Western Blot, Enzyme-linked Immunosorbent Assay, Staining, TUNEL Assay, Standard Deviation

Journal: Frontiers in Immunology

Article Title: SLC31A1 knockdown mitigates post-MI heart failure via regulation of copper metabolism

doi: 10.3389/fimmu.2026.1707203

Figure Lengend Snippet: SLC31A1 silencing or ATTM suppresses cuproptosis and inflammatory responses in hypoxia-induced macrophages. (A) Cell viability assessed by CCK-8; (B–D) The Cu 2+ level, ATP content, and SDH activity in RAW264.7 cells determined by kits; (E) Levels of cuproptosis-related proteins FDX1 and DLAT in RAW264.7 cells measured by western blot; (F) Mitochondrial damage in cells assessed by TEM; (G) The LDH activity in RAW264.7 cell supernatants detected by the kit; (H-J) Levels of HMGB1, IL-1β, and TNF-α in RAW264.7 cell supernatants measured by ELISA; (K) SLC31A1 mRNA expression determined by RT-qPCR; (L) The SLC31A1 protein level measured by western blot. All cell-based in vitro experiments were independently repeated three times. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Levels of N-terminal pro-brain natriuretic peptide (NT-proBNP), IL-1β, tumor necrosis factor-α (TNF-α) and HMGB1 were measured in the mouse serum and cell supernatants using ELISA kits (Elabscience) (NT-proBNP kit: E-EL-M0834; IL-1β kit: E-EL-M0037; TNF-α kit: E-EL-M3063; HMGB1 kit: E-EL-M0676).

Techniques: CCK-8 Assay, Activity Assay, Western Blot, Enzyme-linked Immunosorbent Assay, Expressing, Quantitative RT-PCR, In Vitro, Standard Deviation

Journal: Frontiers in Immunology

Article Title: SLC31A1 knockdown mitigates post-MI heart failure via regulation of copper metabolism

doi: 10.3389/fimmu.2026.1707203

Figure Lengend Snippet: SLC31A1 is implicated in cuproptosis in macrophages through regulation of the NLRP3/HMGB1 pathway. (A) NLRP3 mRNA expression determined by RT-qPCR; (B) NLRP3, cleaved caspase-1 and ASC protein levels measured by western blot; (C) Cell viability evaluated by CCK-8; (D-F) The Cu 2+ level, ATP content, and SDH activity in RAW264.7 cells assessed by kits; (G) Levels of cuproptosis-related proteins FDX1 and DLAT in RAW264.7 cells determined by western blot; (H) Mitochondrial damage in cells assessed by TEM; (I) The LDH activity in RAW264.7 cell supernatants detected by a kit; (J-L) Levels of HMGB1, IL-1β, and TNF-α in RAW264.7 cell supernatants measured by ELISA. All cell-based in vitro experiments were independently repeated three times. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Levels of N-terminal pro-brain natriuretic peptide (NT-proBNP), IL-1β, tumor necrosis factor-α (TNF-α) and HMGB1 were measured in the mouse serum and cell supernatants using ELISA kits (Elabscience) (NT-proBNP kit: E-EL-M0834; IL-1β kit: E-EL-M0037; TNF-α kit: E-EL-M3063; HMGB1 kit: E-EL-M0676).

Techniques: Expressing, Quantitative RT-PCR, Western Blot, CCK-8 Assay, Activity Assay, Enzyme-linked Immunosorbent Assay, In Vitro, Standard Deviation

Journal: Frontiers in Immunology

Article Title: SLC31A1 knockdown mitigates post-MI heart failure via regulation of copper metabolism

doi: 10.3389/fimmu.2026.1707203

Figure Lengend Snippet: Activation of the NLRP3/HMGB1 pathway partly counteracts the protection against macrophage cuproptosis and cardiomyocyte apoptosis mediated by SLC31A1 knockdown in mice with post-AMI HF. (A) NLRP3 mRNA expression in mouse macrophages determined by RT-qPCR, n = 12; (B) NLRP3, cleaved caspase-1 and ASC protein levels in mouse macrophages measured by western blot, n = 12; (C-E) The Cu 2+ level, ATP content, and SDH activity in mouse macrophages assessed by kits, n = 12; (F) Levels of cuproptosis-related proteins FDX1 and DLAT in mouse macrophages determined by western blot, n = 12; (G) Mitochondrial damage in cells assessed by TEM; (H-J) Levels of HMGB1, IL-1β, and TNF-α in mouse serum measured by ELISA, n = 12; (K-L) LVEF and LVEDP detected by echocardiography, n = 12; (M) The NT-proBNP level in mouse serum measured by ELISA, n = 12; (N) Representative images of TTC-stained heart sections and quantification of myocardial infarction, n = 6; (O) Cardiomyocyte apoptosis evaluated by TUNEL staining, n = 6. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Levels of N-terminal pro-brain natriuretic peptide (NT-proBNP), IL-1β, tumor necrosis factor-α (TNF-α) and HMGB1 were measured in the mouse serum and cell supernatants using ELISA kits (Elabscience) (NT-proBNP kit: E-EL-M0834; IL-1β kit: E-EL-M0037; TNF-α kit: E-EL-M3063; HMGB1 kit: E-EL-M0676).

Techniques: Activation Assay, Knockdown, Expressing, Quantitative RT-PCR, Western Blot, Activity Assay, Enzyme-linked Immunosorbent Assay, Staining, TUNEL Assay, Standard Deviation