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PEDV infection reprograms host metabolism toward aerobic glycolysis. ST cells were infected with PEDV at an MOI of 1 for 24 h. (A) Metabolic heatmap showing relative abundance of glycolytic and TCA cycle metabolites in mock- and PEDV-infected cells. Metabolomic data were obtained from four biological replicates per group. Metabolite levels were normalized to mock controls. (B–C) Protein expression of key glycolytic regulators <t>(GLUT1,</t> HK2, PFKM, PFKFB3, and LDHA) and PEDV N protein was analyzed by western blots. β-Tubulin was used as a control. (D–E) Glucose uptake was measured by flow cytometry and quantified as mean fluorescence intensity (MFI). (F) Lactate production was quantified using a lactate assay kit at 24 hpi. (G) Schematic illustration of glucose metabolic reprogramming during PEDV infection, with upregulated metabolites indicated in red and downregulated metabolites in green. Data were presented as mean ± SEM from three independent experiments. ∗ P < 0.05, ∗∗ P < 0.01.
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Electroacupuncture inhibits abnormal expression of microvessels and inflammation‐related proteins in APP/PS1 mice. (A) Representative immunoblots of PDGFRβ and CD31 expression in the prefrontal cortex. (B) Representative immunoblots of PDGFRβ, CD31, and <t>GLUT1</t> expression in the hippocampus. (C) Representative immunoblots of Occludin, Claudin‐5, ZO‐1, NF‐κB, TNF‐α, and IL‐1β expression in the hippocampus. (D) Quantitative data of PDGFRβ and CD31 expression in the prefrontal cortex. (E) Quantitative data of PDGFRβ, CD31, and GLUT1 expression in the hippocampus. (F) Quantitative analysis of Occludin, Claudin‐5, and ZO‐1 expression in the hippocampus. (G) Quantitative analysis of NF‐κB, TNF‐α, and IL‐1β expression in the hippocampus. Data are expressed as mean ± SEM ( n = 3 per group). * p < 0.05 between groups. (one‐way ANOVA followed by Tukey test).
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Electroacupuncture inhibits abnormal expression of microvessels and inflammation‐related proteins in APP/PS1 mice. (A) Representative immunoblots of PDGFRβ and CD31 expression in the prefrontal cortex. (B) Representative immunoblots of PDGFRβ, CD31, and <t>GLUT1</t> expression in the hippocampus. (C) Representative immunoblots of Occludin, Claudin‐5, ZO‐1, NF‐κB, TNF‐α, and IL‐1β expression in the hippocampus. (D) Quantitative data of PDGFRβ and CD31 expression in the prefrontal cortex. (E) Quantitative data of PDGFRβ, CD31, and GLUT1 expression in the hippocampus. (F) Quantitative analysis of Occludin, Claudin‐5, and ZO‐1 expression in the hippocampus. (G) Quantitative analysis of NF‐κB, TNF‐α, and IL‐1β expression in the hippocampus. Data are expressed as mean ± SEM ( n = 3 per group). * p < 0.05 between groups. (one‐way ANOVA followed by Tukey test).
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Electroacupuncture inhibits abnormal expression of microvessels and inflammation‐related proteins in APP/PS1 mice. (A) Representative immunoblots of PDGFRβ and CD31 expression in the prefrontal cortex. (B) Representative immunoblots of PDGFRβ, CD31, and <t>GLUT1</t> expression in the hippocampus. (C) Representative immunoblots of Occludin, Claudin‐5, ZO‐1, NF‐κB, TNF‐α, and IL‐1β expression in the hippocampus. (D) Quantitative data of PDGFRβ and CD31 expression in the prefrontal cortex. (E) Quantitative data of PDGFRβ, CD31, and GLUT1 expression in the hippocampus. (F) Quantitative analysis of Occludin, Claudin‐5, and ZO‐1 expression in the hippocampus. (G) Quantitative analysis of NF‐κB, TNF‐α, and IL‐1β expression in the hippocampus. Data are expressed as mean ± SEM ( n = 3 per group). * p < 0.05 between groups. (one‐way ANOVA followed by Tukey test).
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Electroacupuncture inhibits abnormal expression of microvessels and inflammation‐related proteins in APP/PS1 mice. (A) Representative immunoblots of PDGFRβ and CD31 expression in the prefrontal cortex. (B) Representative immunoblots of PDGFRβ, CD31, and <t>GLUT1</t> expression in the hippocampus. (C) Representative immunoblots of Occludin, Claudin‐5, ZO‐1, NF‐κB, TNF‐α, and IL‐1β expression in the hippocampus. (D) Quantitative data of PDGFRβ and CD31 expression in the prefrontal cortex. (E) Quantitative data of PDGFRβ, CD31, and GLUT1 expression in the hippocampus. (F) Quantitative analysis of Occludin, Claudin‐5, and ZO‐1 expression in the hippocampus. (G) Quantitative analysis of NF‐κB, TNF‐α, and IL‐1β expression in the hippocampus. Data are expressed as mean ± SEM ( n = 3 per group). * p < 0.05 between groups. (one‐way ANOVA followed by Tukey test).
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Image Search Results


PEDV infection reprograms host metabolism toward aerobic glycolysis. ST cells were infected with PEDV at an MOI of 1 for 24 h. (A) Metabolic heatmap showing relative abundance of glycolytic and TCA cycle metabolites in mock- and PEDV-infected cells. Metabolomic data were obtained from four biological replicates per group. Metabolite levels were normalized to mock controls. (B–C) Protein expression of key glycolytic regulators (GLUT1, HK2, PFKM, PFKFB3, and LDHA) and PEDV N protein was analyzed by western blots. β-Tubulin was used as a control. (D–E) Glucose uptake was measured by flow cytometry and quantified as mean fluorescence intensity (MFI). (F) Lactate production was quantified using a lactate assay kit at 24 hpi. (G) Schematic illustration of glucose metabolic reprogramming during PEDV infection, with upregulated metabolites indicated in red and downregulated metabolites in green. Data were presented as mean ± SEM from three independent experiments. ∗ P < 0.05, ∗∗ P < 0.01.

Journal: Redox Biology

Article Title: Porcine epidemic diarrhea virus promotes viral replication via ROS/HIF-1α-mediated glycolysis

doi: 10.1016/j.redox.2026.104008

Figure Lengend Snippet: PEDV infection reprograms host metabolism toward aerobic glycolysis. ST cells were infected with PEDV at an MOI of 1 for 24 h. (A) Metabolic heatmap showing relative abundance of glycolytic and TCA cycle metabolites in mock- and PEDV-infected cells. Metabolomic data were obtained from four biological replicates per group. Metabolite levels were normalized to mock controls. (B–C) Protein expression of key glycolytic regulators (GLUT1, HK2, PFKM, PFKFB3, and LDHA) and PEDV N protein was analyzed by western blots. β-Tubulin was used as a control. (D–E) Glucose uptake was measured by flow cytometry and quantified as mean fluorescence intensity (MFI). (F) Lactate production was quantified using a lactate assay kit at 24 hpi. (G) Schematic illustration of glucose metabolic reprogramming during PEDV infection, with upregulated metabolites indicated in red and downregulated metabolites in green. Data were presented as mean ± SEM from three independent experiments. ∗ P < 0.05, ∗∗ P < 0.01.

Article Snippet: Glucose Transporter 1 (GLUT1) polyclonal antibody (GLUT1; 21829-1-AP), Hexokinase 2 polyclonal antibody (HK2; 22029-1-AP), phosphofructokinase (PFKM) polyclonal antibody (PFKM; 55028-1-AP), 6-phosphofructo-2-kinase (PFKFB3) polyclonal antibody (PFKFB3; 13763-1-AP), and lactate dehydrogenase A (LDHA)-specific polyclonal antibody (LDHA; 19987-1-AP) were purchased from Proteintech (China).

Techniques: Infection, Metabolomic, Expressing, Western Blot, Control, Flow Cytometry, Fluorescence, Lactate Assay

Electroacupuncture inhibits abnormal expression of microvessels and inflammation‐related proteins in APP/PS1 mice. (A) Representative immunoblots of PDGFRβ and CD31 expression in the prefrontal cortex. (B) Representative immunoblots of PDGFRβ, CD31, and GLUT1 expression in the hippocampus. (C) Representative immunoblots of Occludin, Claudin‐5, ZO‐1, NF‐κB, TNF‐α, and IL‐1β expression in the hippocampus. (D) Quantitative data of PDGFRβ and CD31 expression in the prefrontal cortex. (E) Quantitative data of PDGFRβ, CD31, and GLUT1 expression in the hippocampus. (F) Quantitative analysis of Occludin, Claudin‐5, and ZO‐1 expression in the hippocampus. (G) Quantitative analysis of NF‐κB, TNF‐α, and IL‐1β expression in the hippocampus. Data are expressed as mean ± SEM ( n = 3 per group). * p < 0.05 between groups. (one‐way ANOVA followed by Tukey test).

Journal: CNS Neuroscience & Therapeutics

Article Title: Electroacupuncture Prevents Against AD‐Like Phenotypes in APP/PS1 Mice: Investigation of the Mechanisms From Cerebral Microangiopathy

doi: 10.1002/cns.70696

Figure Lengend Snippet: Electroacupuncture inhibits abnormal expression of microvessels and inflammation‐related proteins in APP/PS1 mice. (A) Representative immunoblots of PDGFRβ and CD31 expression in the prefrontal cortex. (B) Representative immunoblots of PDGFRβ, CD31, and GLUT1 expression in the hippocampus. (C) Representative immunoblots of Occludin, Claudin‐5, ZO‐1, NF‐κB, TNF‐α, and IL‐1β expression in the hippocampus. (D) Quantitative data of PDGFRβ and CD31 expression in the prefrontal cortex. (E) Quantitative data of PDGFRβ, CD31, and GLUT1 expression in the hippocampus. (F) Quantitative analysis of Occludin, Claudin‐5, and ZO‐1 expression in the hippocampus. (G) Quantitative analysis of NF‐κB, TNF‐α, and IL‐1β expression in the hippocampus. Data are expressed as mean ± SEM ( n = 3 per group). * p < 0.05 between groups. (one‐way ANOVA followed by Tukey test).

Article Snippet: After blocking with 5% non‐fat milk for 2 h at room temperature, the membranes were incubated with primary antibodies overnight at 4°C: GAPDH (1:1000, BM3874, Boster, China), platelet‐derived growth factor receptor beta (PDGFRβ) (1:1000, A00096‐1, Boster, China), Zonula occludens‐1 (ZO‐1) (1:1000, PB9234, Boster, China), Claudin 5 (1:1000, 29,767–1‐AP, Proteintech, China), Occludin (1:1000, A01246‐4, Boster, China), NF‐κB (1:1000, CY5034, Abways, China), TNF‐α (1:1000, RM8040, Biodragon, China), IL‐1β (1:1000, CY5087, Abways, China), BDNF (1:1000, E17G19, Selleck, China), PSD95 (1:1000, F17C8, Selleck, China), CD31 (1:1000, 11,265–1‐AP, Proteintech, China), glucose transporters 1 (GLUT1) (1:1000, P22E15, Selleck, China).

Techniques: Expressing, Western Blot