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acetyl coa elisa kit  (Elabscience Biotechnology)


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    Elabscience Biotechnology acetyl coa elisa kit
    Analysis of glycolysis-associated metabolite level changes in MCF-7 and MDA-MB-231 breast cancer cells. Levels of (A) PGK2, (B) pyruvate and <t>(C)</t> <t>acetyl-CoA</t> in MCF-7 cells, and (D) PGK2, (E) pyruvate and (F) acetyl-CoA in MDA-MB-231 cells transfected with vector control, PINK1-OE or PINK1-OE + siPGK2. Quantitative analysis was performed using <t>ELISA</t> in cells under the three indicated conditions. Statistical analysis was performed using a one-way ANOVA followed by Tukey's post-hoc test. Data are represented as the mean ± SEM from at least three independent experiments. ***P<0.001. PGK2, phosphoglycerate kinase 2; PINK1, PTEN-induced kinase 1; OE, overexpression; si, small interfering.
    Acetyl Coa Elisa Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "PINK1-mediated mitophagy enhances breast cancer proliferation through metabolic reprogramming"

    Article Title: PINK1-mediated mitophagy enhances breast cancer proliferation through metabolic reprogramming

    Journal: Oncology Reports

    doi: 10.3892/or.2026.9117

    Analysis of glycolysis-associated metabolite level changes in MCF-7 and MDA-MB-231 breast cancer cells. Levels of (A) PGK2, (B) pyruvate and (C) acetyl-CoA in MCF-7 cells, and (D) PGK2, (E) pyruvate and (F) acetyl-CoA in MDA-MB-231 cells transfected with vector control, PINK1-OE or PINK1-OE + siPGK2. Quantitative analysis was performed using ELISA in cells under the three indicated conditions. Statistical analysis was performed using a one-way ANOVA followed by Tukey's post-hoc test. Data are represented as the mean ± SEM from at least three independent experiments. ***P<0.001. PGK2, phosphoglycerate kinase 2; PINK1, PTEN-induced kinase 1; OE, overexpression; si, small interfering.
    Figure Legend Snippet: Analysis of glycolysis-associated metabolite level changes in MCF-7 and MDA-MB-231 breast cancer cells. Levels of (A) PGK2, (B) pyruvate and (C) acetyl-CoA in MCF-7 cells, and (D) PGK2, (E) pyruvate and (F) acetyl-CoA in MDA-MB-231 cells transfected with vector control, PINK1-OE or PINK1-OE + siPGK2. Quantitative analysis was performed using ELISA in cells under the three indicated conditions. Statistical analysis was performed using a one-way ANOVA followed by Tukey's post-hoc test. Data are represented as the mean ± SEM from at least three independent experiments. ***P<0.001. PGK2, phosphoglycerate kinase 2; PINK1, PTEN-induced kinase 1; OE, overexpression; si, small interfering.

    Techniques Used: Transfection, Plasmid Preparation, Control, Enzyme-linked Immunosorbent Assay, Over Expression



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    Elabscience Biotechnology acetyl coa elisa kit
    Analysis of glycolysis-associated metabolite level changes in MCF-7 and MDA-MB-231 breast cancer cells. Levels of (A) PGK2, (B) pyruvate and <t>(C)</t> <t>acetyl-CoA</t> in MCF-7 cells, and (D) PGK2, (E) pyruvate and (F) acetyl-CoA in MDA-MB-231 cells transfected with vector control, PINK1-OE or PINK1-OE + siPGK2. Quantitative analysis was performed using <t>ELISA</t> in cells under the three indicated conditions. Statistical analysis was performed using a one-way ANOVA followed by Tukey's post-hoc test. Data are represented as the mean ± SEM from at least three independent experiments. ***P<0.001. PGK2, phosphoglycerate kinase 2; PINK1, PTEN-induced kinase 1; OE, overexpression; si, small interfering.
    Acetyl Coa Elisa Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Elabscience Biotechnology acetyl coa assay kit
    Analysis of glycolysis-associated metabolite level changes in MCF-7 and MDA-MB-231 breast cancer cells. Levels of (A) PGK2, (B) pyruvate and <t>(C)</t> <t>acetyl-CoA</t> in MCF-7 cells, and (D) PGK2, (E) pyruvate and (F) acetyl-CoA in MDA-MB-231 cells transfected with vector control, PINK1-OE or PINK1-OE + siPGK2. Quantitative analysis was performed using <t>ELISA</t> in cells under the three indicated conditions. Statistical analysis was performed using a one-way ANOVA followed by Tukey's post-hoc test. Data are represented as the mean ± SEM from at least three independent experiments. ***P<0.001. PGK2, phosphoglycerate kinase 2; PINK1, PTEN-induced kinase 1; OE, overexpression; si, small interfering.
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    ( A ) Schematic illustrating glucose-derived citrate export and <t>ACLY-dependent</t> <t>acetyl-CoA</t> production linking metabolism to histone acetylation. ( B ) Relative abundance of citric acid in Veh and STZ placentas on D18 detected by LC-MS. ( C ) Quantification of Acetyl-CoA concentration in Veh and STZ placentas on D18. Data represent the mean ± SEM. Two-tailed unpaired Student’s t-test. P =0.0165. ( D ) Representative BODIPY staining in Veh and STZ placentas on D18. Scale bar, 50μm. ( E ) Immunoblotting analysis of histone acetylation marks (H3K27ac, H3K9ac, H3K14ac, H3K18ac, and total H3ac) in Veh and STZ placentas on D18 with total H3 as a loading control. ( F ) Representative immunofluorescence staining of H3K27ac in Veh and STZ placentas on D18. Scale bar, 20μm.
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    Elabscience Biotechnology acetyl coa a coa elisa kit manual
    Inhibition of HDAC1/2 enhanced fatty acid oxidation in microglia. (A) Schematic diagram of untargeted metabolomics in BV2 cells following 24 h of Hemin stimulation, by figdraw . (B) PCA plot of untargeted metabolomics for three groups of BV2 cells. n = 6 to 8 per group. (C) Bar chart of differential metabolites diagram. RT‐qPCR of key enzymes involved in fatty acid oxidation. n = 3 per group. (D) Volcano plot of differential metabolites between BV2+Hemin and BV2+Hemin +FK228. (E) Venn diagram of the intersection of differentially expressed metabolites between BV2 vs. BV2+Hemin and BV2+Hemin vs. BV2+Hemin+FK228. (F) Enrichment analysis of the differentially metabolites between BV2+Hemin and BV2+Hemin+FK228 in KEGG pathway. (G) Heatmap of key enzymes involved in fatty acid biosynthesis and fatty acid oxidation. (H) RT‐qPCR validation of the differentially expressed genes of fatty acid oxidation and biosynthesis. n = 3 per group. (I) GSEA analysis of mitochondrial long chain fatty acid β‐oxidation. (J) Flow cytometry detection of neutral lipid content in BV2 cells (labeled with BODIPY493/503 probe) representative figure, as reflected by the quantification (K). n = 3 per group. (L) Detection <t>of</t> <t>acetyl‐CoA</t> content in BV2 cells using <t>ELISA</t> following 24 h of Hemin stimulation. n = 3 per group. (M) Detection of free fatty acids content in BV2 cells following 24 h of Hemin stimulation. n = 3 per group. (N) Schematic diagram of enhanced fatty acid oxidation, by figdraw . (O) Representative images of Iba1/Bodipy‐493/503 (labeling lipid droplet) immunostaining around the hematoma, as reflected by the quantification (P). n = 5 mice per group. All values are expressed as mean ± SD. The data were analyzed using one‐way analysis of variance (ANOVA) followed by Bonferroni's post hoc test (H, K, L, M) or unpaired two‐tailed Student's t test (P). * p < 0.05, ** p < 0.01, *** p < 0.001 ns, not significant.
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    Inhibition of HDAC1/2 enhanced fatty acid oxidation in microglia. (A) Schematic diagram of untargeted metabolomics in BV2 cells following 24 h of Hemin stimulation, by figdraw . (B) PCA plot of untargeted metabolomics for three groups of BV2 cells. n = 6 to 8 per group. (C) Bar chart of differential metabolites diagram. RT‐qPCR of key enzymes involved in fatty acid oxidation. n = 3 per group. (D) Volcano plot of differential metabolites between BV2+Hemin and BV2+Hemin +FK228. (E) Venn diagram of the intersection of differentially expressed metabolites between BV2 vs. BV2+Hemin and BV2+Hemin vs. BV2+Hemin+FK228. (F) Enrichment analysis of the differentially metabolites between BV2+Hemin and BV2+Hemin+FK228 in KEGG pathway. (G) Heatmap of key enzymes involved in fatty acid biosynthesis and fatty acid oxidation. (H) RT‐qPCR validation of the differentially expressed genes of fatty acid oxidation and biosynthesis. n = 3 per group. (I) GSEA analysis of mitochondrial long chain fatty acid β‐oxidation. (J) Flow cytometry detection of neutral lipid content in BV2 cells (labeled with BODIPY493/503 probe) representative figure, as reflected by the quantification (K). n = 3 per group. (L) Detection <t>of</t> <t>acetyl‐CoA</t> content in BV2 cells using <t>ELISA</t> following 24 h of Hemin stimulation. n = 3 per group. (M) Detection of free fatty acids content in BV2 cells following 24 h of Hemin stimulation. n = 3 per group. (N) Schematic diagram of enhanced fatty acid oxidation, by figdraw . (O) Representative images of Iba1/Bodipy‐493/503 (labeling lipid droplet) immunostaining around the hematoma, as reflected by the quantification (P). n = 5 mice per group. All values are expressed as mean ± SD. The data were analyzed using one‐way analysis of variance (ANOVA) followed by Bonferroni's post hoc test (H, K, L, M) or unpaired two‐tailed Student's t test (P). * p < 0.05, ** p < 0.01, *** p < 0.001 ns, not significant.
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    Inhibition of HDAC1/2 enhanced fatty acid oxidation in microglia. (A) Schematic diagram of untargeted metabolomics in BV2 cells following 24 h of Hemin stimulation, by figdraw . (B) PCA plot of untargeted metabolomics for three groups of BV2 cells. n = 6 to 8 per group. (C) Bar chart of differential metabolites diagram. RT‐qPCR of key enzymes involved in fatty acid oxidation. n = 3 per group. (D) Volcano plot of differential metabolites between BV2+Hemin and BV2+Hemin +FK228. (E) Venn diagram of the intersection of differentially expressed metabolites between BV2 vs. BV2+Hemin and BV2+Hemin vs. BV2+Hemin+FK228. (F) Enrichment analysis of the differentially metabolites between BV2+Hemin and BV2+Hemin+FK228 in KEGG pathway. (G) Heatmap of key enzymes involved in fatty acid biosynthesis and fatty acid oxidation. (H) RT‐qPCR validation of the differentially expressed genes of fatty acid oxidation and biosynthesis. n = 3 per group. (I) GSEA analysis of mitochondrial long chain fatty acid β‐oxidation. (J) Flow cytometry detection of neutral lipid content in BV2 cells (labeled with BODIPY493/503 probe) representative figure, as reflected by the quantification (K). n = 3 per group. (L) Detection <t>of</t> <t>acetyl‐CoA</t> content in BV2 cells using <t>ELISA</t> following 24 h of Hemin stimulation. n = 3 per group. (M) Detection of free fatty acids content in BV2 cells following 24 h of Hemin stimulation. n = 3 per group. (N) Schematic diagram of enhanced fatty acid oxidation, by figdraw . (O) Representative images of Iba1/Bodipy‐493/503 (labeling lipid droplet) immunostaining around the hematoma, as reflected by the quantification (P). n = 5 mice per group. All values are expressed as mean ± SD. The data were analyzed using one‐way analysis of variance (ANOVA) followed by Bonferroni's post hoc test (H, K, L, M) or unpaired two‐tailed Student's t test (P). * p < 0.05, ** p < 0.01, *** p < 0.001 ns, not significant.
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    Image Search Results


    Analysis of glycolysis-associated metabolite level changes in MCF-7 and MDA-MB-231 breast cancer cells. Levels of (A) PGK2, (B) pyruvate and (C) acetyl-CoA in MCF-7 cells, and (D) PGK2, (E) pyruvate and (F) acetyl-CoA in MDA-MB-231 cells transfected with vector control, PINK1-OE or PINK1-OE + siPGK2. Quantitative analysis was performed using ELISA in cells under the three indicated conditions. Statistical analysis was performed using a one-way ANOVA followed by Tukey's post-hoc test. Data are represented as the mean ± SEM from at least three independent experiments. ***P<0.001. PGK2, phosphoglycerate kinase 2; PINK1, PTEN-induced kinase 1; OE, overexpression; si, small interfering.

    Journal: Oncology Reports

    Article Title: PINK1-mediated mitophagy enhances breast cancer proliferation through metabolic reprogramming

    doi: 10.3892/or.2026.9117

    Figure Lengend Snippet: Analysis of glycolysis-associated metabolite level changes in MCF-7 and MDA-MB-231 breast cancer cells. Levels of (A) PGK2, (B) pyruvate and (C) acetyl-CoA in MCF-7 cells, and (D) PGK2, (E) pyruvate and (F) acetyl-CoA in MDA-MB-231 cells transfected with vector control, PINK1-OE or PINK1-OE + siPGK2. Quantitative analysis was performed using ELISA in cells under the three indicated conditions. Statistical analysis was performed using a one-way ANOVA followed by Tukey's post-hoc test. Data are represented as the mean ± SEM from at least three independent experiments. ***P<0.001. PGK2, phosphoglycerate kinase 2; PINK1, PTEN-induced kinase 1; OE, overexpression; si, small interfering.

    Article Snippet: Acetyl-CoA content was assessed using the Acetyl-CoA ELISA Kit (Wuhan Elabscience Biotechnology Co., Ltd.; cat. no. E-BC-F046-48T-ELS).

    Techniques: Transfection, Plasmid Preparation, Control, Enzyme-linked Immunosorbent Assay, Over Expression

    ( A ) Schematic illustrating glucose-derived citrate export and ACLY-dependent acetyl-CoA production linking metabolism to histone acetylation. ( B ) Relative abundance of citric acid in Veh and STZ placentas on D18 detected by LC-MS. ( C ) Quantification of Acetyl-CoA concentration in Veh and STZ placentas on D18. Data represent the mean ± SEM. Two-tailed unpaired Student’s t-test. P =0.0165. ( D ) Representative BODIPY staining in Veh and STZ placentas on D18. Scale bar, 50μm. ( E ) Immunoblotting analysis of histone acetylation marks (H3K27ac, H3K9ac, H3K14ac, H3K18ac, and total H3ac) in Veh and STZ placentas on D18 with total H3 as a loading control. ( F ) Representative immunofluorescence staining of H3K27ac in Veh and STZ placentas on D18. Scale bar, 20μm.

    Journal: bioRxiv

    Article Title: Metabolic adaptation to maternal hyperglycemia via ACLY-dependent acetyl-CoA production drives epigenetic remodeling and dysregulated placental development

    doi: 10.64898/2026.03.17.712507

    Figure Lengend Snippet: ( A ) Schematic illustrating glucose-derived citrate export and ACLY-dependent acetyl-CoA production linking metabolism to histone acetylation. ( B ) Relative abundance of citric acid in Veh and STZ placentas on D18 detected by LC-MS. ( C ) Quantification of Acetyl-CoA concentration in Veh and STZ placentas on D18. Data represent the mean ± SEM. Two-tailed unpaired Student’s t-test. P =0.0165. ( D ) Representative BODIPY staining in Veh and STZ placentas on D18. Scale bar, 50μm. ( E ) Immunoblotting analysis of histone acetylation marks (H3K27ac, H3K9ac, H3K14ac, H3K18ac, and total H3ac) in Veh and STZ placentas on D18 with total H3 as a loading control. ( F ) Representative immunofluorescence staining of H3K27ac in Veh and STZ placentas on D18. Scale bar, 20μm.

    Article Snippet: Placental acetyl-CoA levels were measured using a commercial acetyl-CoA ELISA kit (Sangon Biotech, D751001).

    Techniques: Derivative Assay, Liquid Chromatography with Mass Spectroscopy, Concentration Assay, Two Tailed Test, Staining, Western Blot, Control, Immunofluorescence

    ( A ) Heatmap of representative OXPHOS related genes in Veh and STZ placentas on D18. ( B ) Heatmap of representative FA biosynthesis related genes in Veh and STZ placentas on D18. ( C ) Schematic of citrate-to-acetyl-CoA conversion by ACLY. ( D ) RT-qPCR analysis of Acly in Veh and STZ placentas on D18. The values are normalized to Actb and indicated as the mean ± SEM. ** P <0.01. ( E ) Representative immunofluorescence staining of ACLY in Veh and STZ placentas on D18. Scale bars, 100μm. ( F ) Immunoblotting analysis of ACLY in Veh and STZ placentas on D18 with β-actin as a loading control. ( G ) Densitometric quantification of ACLY normalized to β-actin in Veh and STZ placentas on D18. Data represent the mean ± SEM. Two-tailed unpaired Student’s t-test, *** P < 0.001.

    Journal: bioRxiv

    Article Title: Metabolic adaptation to maternal hyperglycemia via ACLY-dependent acetyl-CoA production drives epigenetic remodeling and dysregulated placental development

    doi: 10.64898/2026.03.17.712507

    Figure Lengend Snippet: ( A ) Heatmap of representative OXPHOS related genes in Veh and STZ placentas on D18. ( B ) Heatmap of representative FA biosynthesis related genes in Veh and STZ placentas on D18. ( C ) Schematic of citrate-to-acetyl-CoA conversion by ACLY. ( D ) RT-qPCR analysis of Acly in Veh and STZ placentas on D18. The values are normalized to Actb and indicated as the mean ± SEM. ** P <0.01. ( E ) Representative immunofluorescence staining of ACLY in Veh and STZ placentas on D18. Scale bars, 100μm. ( F ) Immunoblotting analysis of ACLY in Veh and STZ placentas on D18 with β-actin as a loading control. ( G ) Densitometric quantification of ACLY normalized to β-actin in Veh and STZ placentas on D18. Data represent the mean ± SEM. Two-tailed unpaired Student’s t-test, *** P < 0.001.

    Article Snippet: Placental acetyl-CoA levels were measured using a commercial acetyl-CoA ELISA kit (Sangon Biotech, D751001).

    Techniques: Quantitative RT-PCR, Immunofluorescence, Staining, Western Blot, Control, Two Tailed Test

    ( A ) Clinical characteristics of participants including age, pre-pregnancy BMI, HbA1c, OGTT (0 h, 1 h, 2 h), neonatal birth weight, SGA, LGA, and NICU in normal and GDM groups. Values are mean ± SD or n/N (%). Continuous variables were compared using unpaired two-tailed t tests. Categorical variables were compared using Fisher’s exact tests. ns, not significant. ( B ) Neonatal birth weight in normal and GDM groups. Data represent the mean. Two-tailed unpaired Student’s t-test. ns, not significant. ( C–E ) Rates of SGA ( C ), LGA ( D ), and NICU admission ( E ) in normal and GDM groups, shown as n/N (%). ( F ) Representative immunofluorescence images of ACLY and hCG with nuclei counterstained by Hoechst in normal and GDM term placental villis. Scale bar, 100μm. ( G ) Quantification of acetyl-CoA concentration in term placental tissues from normal and GDM. Data represent the mean ± SEM. Two-tailed unpaired Student’s t-test. * P < 0.05. ( H ) Representative immunoblots of H3K27ac/ H3K9ac and ACLY in term placental tissues from normal and GDM. Total H3 and β-actin serve as loading controls.

    Journal: bioRxiv

    Article Title: Metabolic adaptation to maternal hyperglycemia via ACLY-dependent acetyl-CoA production drives epigenetic remodeling and dysregulated placental development

    doi: 10.64898/2026.03.17.712507

    Figure Lengend Snippet: ( A ) Clinical characteristics of participants including age, pre-pregnancy BMI, HbA1c, OGTT (0 h, 1 h, 2 h), neonatal birth weight, SGA, LGA, and NICU in normal and GDM groups. Values are mean ± SD or n/N (%). Continuous variables were compared using unpaired two-tailed t tests. Categorical variables were compared using Fisher’s exact tests. ns, not significant. ( B ) Neonatal birth weight in normal and GDM groups. Data represent the mean. Two-tailed unpaired Student’s t-test. ns, not significant. ( C–E ) Rates of SGA ( C ), LGA ( D ), and NICU admission ( E ) in normal and GDM groups, shown as n/N (%). ( F ) Representative immunofluorescence images of ACLY and hCG with nuclei counterstained by Hoechst in normal and GDM term placental villis. Scale bar, 100μm. ( G ) Quantification of acetyl-CoA concentration in term placental tissues from normal and GDM. Data represent the mean ± SEM. Two-tailed unpaired Student’s t-test. * P < 0.05. ( H ) Representative immunoblots of H3K27ac/ H3K9ac and ACLY in term placental tissues from normal and GDM. Total H3 and β-actin serve as loading controls.

    Article Snippet: Placental acetyl-CoA levels were measured using a commercial acetyl-CoA ELISA kit (Sangon Biotech, D751001).

    Techniques: Two Tailed Test, Immunofluorescence, Concentration Assay, Western Blot

    Inhibition of HDAC1/2 enhanced fatty acid oxidation in microglia. (A) Schematic diagram of untargeted metabolomics in BV2 cells following 24 h of Hemin stimulation, by figdraw . (B) PCA plot of untargeted metabolomics for three groups of BV2 cells. n = 6 to 8 per group. (C) Bar chart of differential metabolites diagram. RT‐qPCR of key enzymes involved in fatty acid oxidation. n = 3 per group. (D) Volcano plot of differential metabolites between BV2+Hemin and BV2+Hemin +FK228. (E) Venn diagram of the intersection of differentially expressed metabolites between BV2 vs. BV2+Hemin and BV2+Hemin vs. BV2+Hemin+FK228. (F) Enrichment analysis of the differentially metabolites between BV2+Hemin and BV2+Hemin+FK228 in KEGG pathway. (G) Heatmap of key enzymes involved in fatty acid biosynthesis and fatty acid oxidation. (H) RT‐qPCR validation of the differentially expressed genes of fatty acid oxidation and biosynthesis. n = 3 per group. (I) GSEA analysis of mitochondrial long chain fatty acid β‐oxidation. (J) Flow cytometry detection of neutral lipid content in BV2 cells (labeled with BODIPY493/503 probe) representative figure, as reflected by the quantification (K). n = 3 per group. (L) Detection of acetyl‐CoA content in BV2 cells using ELISA following 24 h of Hemin stimulation. n = 3 per group. (M) Detection of free fatty acids content in BV2 cells following 24 h of Hemin stimulation. n = 3 per group. (N) Schematic diagram of enhanced fatty acid oxidation, by figdraw . (O) Representative images of Iba1/Bodipy‐493/503 (labeling lipid droplet) immunostaining around the hematoma, as reflected by the quantification (P). n = 5 mice per group. All values are expressed as mean ± SD. The data were analyzed using one‐way analysis of variance (ANOVA) followed by Bonferroni's post hoc test (H, K, L, M) or unpaired two‐tailed Student's t test (P). * p < 0.05, ** p < 0.01, *** p < 0.001 ns, not significant.

    Journal: Advanced Science

    Article Title: Disengaging the Engine: Histone Deacetylases 1 and 2‐Mediated Acetylation of Hexokinase‐2 Regulates Energy Metabolism in Microglia Following Intracerebral Hemorrhage

    doi: 10.1002/advs.202500194

    Figure Lengend Snippet: Inhibition of HDAC1/2 enhanced fatty acid oxidation in microglia. (A) Schematic diagram of untargeted metabolomics in BV2 cells following 24 h of Hemin stimulation, by figdraw . (B) PCA plot of untargeted metabolomics for three groups of BV2 cells. n = 6 to 8 per group. (C) Bar chart of differential metabolites diagram. RT‐qPCR of key enzymes involved in fatty acid oxidation. n = 3 per group. (D) Volcano plot of differential metabolites between BV2+Hemin and BV2+Hemin +FK228. (E) Venn diagram of the intersection of differentially expressed metabolites between BV2 vs. BV2+Hemin and BV2+Hemin vs. BV2+Hemin+FK228. (F) Enrichment analysis of the differentially metabolites between BV2+Hemin and BV2+Hemin+FK228 in KEGG pathway. (G) Heatmap of key enzymes involved in fatty acid biosynthesis and fatty acid oxidation. (H) RT‐qPCR validation of the differentially expressed genes of fatty acid oxidation and biosynthesis. n = 3 per group. (I) GSEA analysis of mitochondrial long chain fatty acid β‐oxidation. (J) Flow cytometry detection of neutral lipid content in BV2 cells (labeled with BODIPY493/503 probe) representative figure, as reflected by the quantification (K). n = 3 per group. (L) Detection of acetyl‐CoA content in BV2 cells using ELISA following 24 h of Hemin stimulation. n = 3 per group. (M) Detection of free fatty acids content in BV2 cells following 24 h of Hemin stimulation. n = 3 per group. (N) Schematic diagram of enhanced fatty acid oxidation, by figdraw . (O) Representative images of Iba1/Bodipy‐493/503 (labeling lipid droplet) immunostaining around the hematoma, as reflected by the quantification (P). n = 5 mice per group. All values are expressed as mean ± SD. The data were analyzed using one‐way analysis of variance (ANOVA) followed by Bonferroni's post hoc test (H, K, L, M) or unpaired two‐tailed Student's t test (P). * p < 0.05, ** p < 0.01, *** p < 0.001 ns, not significant.

    Article Snippet: The following procedure follows the instructions provided in the Acetyl‐CoA (A‐CoA) ELISA Kit manual (Elabscience, E‐EL‐0125).

    Techniques: Inhibition, Quantitative RT-PCR, Biomarker Discovery, Flow Cytometry, Labeling, Enzyme-linked Immunosorbent Assay, Immunostaining, Two Tailed Test