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assay kits  (Elabscience Biotechnology)


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    Elabscience Biotechnology assay kits
    Assay Kits, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 17 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cell+mitochondrial+complex/10__34133_slash_cancomm__0028-265-13-20?v=Elabscience+Biotechnology
    Average 94 stars, based on 17 article reviews
    assay kits - by Bioz Stars, 2026-07
    94/100 stars

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    Elabscience Biotechnology mitochondrial complex iv activity
    LC attenuated myocardial <t>mitochondrial</t> structural damage and respiratory chain abnormalities in EAM mice. (A) Transmission electron microscopy showing morphological changes in mouse heart mitochondria (×5,000, scale bar = 2 μm). Changes in (B) mitochondrial complex IV activity and (C) ATP levels in each group, n = 3. (D,E) DCFH-DA staining flow cytometry to detect ROS levels in each group, n = 3. Data are expressed as Mean ± SEM with individual data points shown. ATP, adenosine triphosphate; ROS, reactive oxygen species.
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    LC attenuated myocardial <t>mitochondrial</t> structural damage and respiratory chain abnormalities in EAM mice. (A) Transmission electron microscopy showing morphological changes in mouse heart mitochondria (×5,000, scale bar = 2 μm). Changes in (B) mitochondrial complex IV activity and (C) ATP levels in each group, n = 3. (D,E) DCFH-DA staining flow cytometry to detect ROS levels in each group, n = 3. Data are expressed as Mean ± SEM with individual data points shown. ATP, adenosine triphosphate; ROS, reactive oxygen species.
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    Elabscience Biotechnology complex v activity assay kit
    293 T cells were transfected with empty vector, wild-type Cend1, or the Cend1-G130P mutant for 48 h, followed by oxygen–glucose deprivation/reoxygenation (OGD/R) treatment. Cells were collected 24 h after reoxygenation for subsequent analyses. A Representative flow cytometric analysis of JC-1 staining showing the proportion of monomers and aggregates. B Quantification of JC-1 monomer proportion. N = 3. C Representative flow cytometric analysis of calcein–cobalt staining to assess mPTP opening. D Quantification of calcein fluorescence intensity. N = 3. E Relative NADH–CoQ reductase (complex I) activity measured using a mitochondrial complex I assay kit. N = 3. F Relative F₁F₀-ATP synthase (complex V) activity measured using a mitochondrial <t>complex</t> <t>V</t> assay kit. N = 3. G Intracellular ATP levels measured by ATP assay kit and normalized to protein content. N = 3. Data are presented as mean ± SEM. * P < 0.05; ** P < 0.01; ns, not significant.
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    Image Search Results


    LC attenuated myocardial mitochondrial structural damage and respiratory chain abnormalities in EAM mice. (A) Transmission electron microscopy showing morphological changes in mouse heart mitochondria (×5,000, scale bar = 2 μm). Changes in (B) mitochondrial complex IV activity and (C) ATP levels in each group, n = 3. (D,E) DCFH-DA staining flow cytometry to detect ROS levels in each group, n = 3. Data are expressed as Mean ± SEM with individual data points shown. ATP, adenosine triphosphate; ROS, reactive oxygen species.

    Journal: Frontiers in Pharmacology

    Article Title: Levocarnitine improves cardiac energy metabolic remodeling in myocarditis mice

    doi: 10.3389/fphar.2025.1706936

    Figure Lengend Snippet: LC attenuated myocardial mitochondrial structural damage and respiratory chain abnormalities in EAM mice. (A) Transmission electron microscopy showing morphological changes in mouse heart mitochondria (×5,000, scale bar = 2 μm). Changes in (B) mitochondrial complex IV activity and (C) ATP levels in each group, n = 3. (D,E) DCFH-DA staining flow cytometry to detect ROS levels in each group, n = 3. Data are expressed as Mean ± SEM with individual data points shown. ATP, adenosine triphosphate; ROS, reactive oxygen species.

    Article Snippet: Mitochondrial complex IV activity was measured with the kit (E-BC-K837-M, Elabscience, Wuhan, China) to assess the integrity of the mitochondrial respiratory chain.

    Techniques: Transmission Assay, Electron Microscopy, Activity Assay, Staining, Flow Cytometry

    LC improves myocardial mitochondrial substrate utilization in EAM mice. (A) Serum H-FABP levels in each group of mice, n = 3. (B–D) Western blot analysis of OCTN-2 and CPT-1B proteins, n = 3. (E) FFA and (F) LAC levels in myocardial tissue from each group of mice, n = 3. Data are expressed as Mean ± SEM with individual data points shown. FABP, heart-type fatty acid-binding protein; OCTN2, organic carnitine transporter novel type 2; CPT-1B, carnitine palmitoyltransferase-1B; FFA, free fatty acid; LAC, lactic acid.

    Journal: Frontiers in Pharmacology

    Article Title: Levocarnitine improves cardiac energy metabolic remodeling in myocarditis mice

    doi: 10.3389/fphar.2025.1706936

    Figure Lengend Snippet: LC improves myocardial mitochondrial substrate utilization in EAM mice. (A) Serum H-FABP levels in each group of mice, n = 3. (B–D) Western blot analysis of OCTN-2 and CPT-1B proteins, n = 3. (E) FFA and (F) LAC levels in myocardial tissue from each group of mice, n = 3. Data are expressed as Mean ± SEM with individual data points shown. FABP, heart-type fatty acid-binding protein; OCTN2, organic carnitine transporter novel type 2; CPT-1B, carnitine palmitoyltransferase-1B; FFA, free fatty acid; LAC, lactic acid.

    Article Snippet: Mitochondrial complex IV activity was measured with the kit (E-BC-K837-M, Elabscience, Wuhan, China) to assess the integrity of the mitochondrial respiratory chain.

    Techniques: Western Blot, Binding Assay

    Pearson’s correlation analysis of p-Akt and PGC-1α with mitochondrial metabolic function. Scatter plots showing the correlation between myocardial p-Akt protein expression and (A) COX IV activity, (B) CPT-1B expression, (C) ROS levels, and (D) ATP. Scatter plots showing the correlation between myocardial PGC-1α protein expression and (E) COX IV activity, (F) CPT-1B expression, (G) ROS levels, and (H) ATP. (n = 9 from 3 groups).

    Journal: Frontiers in Pharmacology

    Article Title: Levocarnitine improves cardiac energy metabolic remodeling in myocarditis mice

    doi: 10.3389/fphar.2025.1706936

    Figure Lengend Snippet: Pearson’s correlation analysis of p-Akt and PGC-1α with mitochondrial metabolic function. Scatter plots showing the correlation between myocardial p-Akt protein expression and (A) COX IV activity, (B) CPT-1B expression, (C) ROS levels, and (D) ATP. Scatter plots showing the correlation between myocardial PGC-1α protein expression and (E) COX IV activity, (F) CPT-1B expression, (G) ROS levels, and (H) ATP. (n = 9 from 3 groups).

    Article Snippet: Mitochondrial complex IV activity was measured with the kit (E-BC-K837-M, Elabscience, Wuhan, China) to assess the integrity of the mitochondrial respiratory chain.

    Techniques: Expressing, Activity Assay

    293 T cells were transfected with empty vector, wild-type Cend1, or the Cend1-G130P mutant for 48 h, followed by oxygen–glucose deprivation/reoxygenation (OGD/R) treatment. Cells were collected 24 h after reoxygenation for subsequent analyses. A Representative flow cytometric analysis of JC-1 staining showing the proportion of monomers and aggregates. B Quantification of JC-1 monomer proportion. N = 3. C Representative flow cytometric analysis of calcein–cobalt staining to assess mPTP opening. D Quantification of calcein fluorescence intensity. N = 3. E Relative NADH–CoQ reductase (complex I) activity measured using a mitochondrial complex I assay kit. N = 3. F Relative F₁F₀-ATP synthase (complex V) activity measured using a mitochondrial complex V assay kit. N = 3. G Intracellular ATP levels measured by ATP assay kit and normalized to protein content. N = 3. Data are presented as mean ± SEM. * P < 0.05; ** P < 0.01; ns, not significant.

    Journal: Communications Biology

    Article Title: Targeting Cend1-Atp5f1b interaction rescues mitochondrial dysfunction and ameliorates ischemic brain injury

    doi: 10.1038/s42003-025-09419-4

    Figure Lengend Snippet: 293 T cells were transfected with empty vector, wild-type Cend1, or the Cend1-G130P mutant for 48 h, followed by oxygen–glucose deprivation/reoxygenation (OGD/R) treatment. Cells were collected 24 h after reoxygenation for subsequent analyses. A Representative flow cytometric analysis of JC-1 staining showing the proportion of monomers and aggregates. B Quantification of JC-1 monomer proportion. N = 3. C Representative flow cytometric analysis of calcein–cobalt staining to assess mPTP opening. D Quantification of calcein fluorescence intensity. N = 3. E Relative NADH–CoQ reductase (complex I) activity measured using a mitochondrial complex I assay kit. N = 3. F Relative F₁F₀-ATP synthase (complex V) activity measured using a mitochondrial complex V assay kit. N = 3. G Intracellular ATP levels measured by ATP assay kit and normalized to protein content. N = 3. Data are presented as mean ± SEM. * P < 0.05; ** P < 0.01; ns, not significant.

    Article Snippet: Activities of mitochondrial complex I and V in 293 T cells were measured using the Cell Mitochondrial Complex I Activity Assay Kit (Elabscience, #E-BC-K834-M) and Complex V Activity Assay Kit (Elabscience, #E-BC-K838-M), respectively, according to the manufacturer’s instructions.

    Techniques: Transfection, Plasmid Preparation, Mutagenesis, Staining, Fluorescence, Activity Assay, ATP Assay

    Cells were collected 24 h after reperfusion for subsequent assays. A Cells were stained with JC-1 at working concentration, and the ratio of JC-1 monomers to aggregates was analyzed by flow cytometry. B Quantification of JC-1 monomer proportion. N = 3. C Cells were stained with MPTP detection reagent at working concentration, and green fluorescence intensity was analyzed by flow cytometry. D Quantification of green fluorescence intensity reflecting mPTP opening. N = 3. E NADH–CoQ reductase activity was measured using a mitochondrial complex I activity assay kit according to the manufacturer’s instructions, and relative activity was quantified. N = 3. F F₁F₀-ATP synthase activity was measured using a complex V activity assay kit and quantified as relative activity. N = 3. G Intracellular ATP content was measured using a luminescence-based ATP assay kit and quantified relative to control. N = 3. Data are presented as mean ± SEM. * P < 0.05; ** P < 0.01; ns, not significant.

    Journal: Communications Biology

    Article Title: Targeting Cend1-Atp5f1b interaction rescues mitochondrial dysfunction and ameliorates ischemic brain injury

    doi: 10.1038/s42003-025-09419-4

    Figure Lengend Snippet: Cells were collected 24 h after reperfusion for subsequent assays. A Cells were stained with JC-1 at working concentration, and the ratio of JC-1 monomers to aggregates was analyzed by flow cytometry. B Quantification of JC-1 monomer proportion. N = 3. C Cells were stained with MPTP detection reagent at working concentration, and green fluorescence intensity was analyzed by flow cytometry. D Quantification of green fluorescence intensity reflecting mPTP opening. N = 3. E NADH–CoQ reductase activity was measured using a mitochondrial complex I activity assay kit according to the manufacturer’s instructions, and relative activity was quantified. N = 3. F F₁F₀-ATP synthase activity was measured using a complex V activity assay kit and quantified as relative activity. N = 3. G Intracellular ATP content was measured using a luminescence-based ATP assay kit and quantified relative to control. N = 3. Data are presented as mean ± SEM. * P < 0.05; ** P < 0.01; ns, not significant.

    Article Snippet: Activities of mitochondrial complex I and V in 293 T cells were measured using the Cell Mitochondrial Complex I Activity Assay Kit (Elabscience, #E-BC-K834-M) and Complex V Activity Assay Kit (Elabscience, #E-BC-K838-M), respectively, according to the manufacturer’s instructions.

    Techniques: Staining, Concentration Assay, Flow Cytometry, Fluorescence, Activity Assay, ATP Assay, Control