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nox2 inhibitor gsk2795039 (MedChemExpress)

Name: nox2 inhibitor gsk2795039
Brand: MedChemExpress
Rating: 95 (80 reviews)

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MedChemExpress nox2 inhibitor gsk2795039

SLC25A28 regulates microglial activation via <t>NOX2‐dependent</t> ROS pathway. (a) CYBB mRNA levels in SLC25A28‐KO versus control microglia (qPCR, n = 3). (b) <t>NOX2</t> <t>protein</t> expression in microglia (Western blot, n = 3). (c) Intracellular ROS levels in microglia assessed by DCFH‐DA staining (scale bar = 5 μm, n = 5). (d) SLC25A28 mRNA expression in overexpression (OE) versus control BV2 cells (qPCR, n = 3). (e) SLC25A28 protein levels in OE and control cells (Western blot, n = 3). (f) Microglial morphology with/without <t>GSK2795039</t> (10 μM) treatment; cell body area was quantified (scale bar = 20 μm, n = 3). (g) Mitochondrial iron visualization using Mito‐FerroGreen staining (scale bar = 5 μm). (h) Quantification of mitochondrial iron content by ferrozine assay ( n = 3). (i) CYBB mRNA expression in OE cells with or without GSK2795039 treatment (qPCR, n = 3). (j) NOX2 protein expression in OE cells with or without GSK2795039 treatment (Western blot, n = 3). (k) ROS levels in OE cells with or without GSK2795039 treatment, measured by DCFH‐DA staining (scale bar = 20 μm, n = 6). (l) Expression of inflammatory markers (iNOS, total caspase‐1, and cleaved caspase‐1) in OE cells with or without GSK2795039 treatment (Western blot, n = 3). (m) ELISA quantification of IL‐1β and TNF‐α in OE cells with or without GSK2795039 treatment ( n = 3). Data are expressed as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

Nox2 Inhibitor Gsk2795039, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 80 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Microglial SLC25A28 Knockout Mitigates Spinal Cord Injury in Mice by Inhibiting Heme Synthesis and Subsequent NOX2 Activation"

Article Title: Microglial SLC25A28 Knockout Mitigates Spinal Cord Injury in Mice by Inhibiting Heme Synthesis and Subsequent NOX2 Activation

Journal: CNS Neuroscience & Therapeutics

doi: 10.1111/cns.70638

SLC25A28 regulates microglial activation via NOX2‐dependent ROS pathway. (a) CYBB mRNA levels in SLC25A28‐KO versus control microglia (qPCR, n = 3). (b) NOX2 protein expression in microglia (Western blot, n = 3). (c) Intracellular ROS levels in microglia assessed by DCFH‐DA staining (scale bar = 5 μm, n = 5). (d) SLC25A28 mRNA expression in overexpression (OE) versus control BV2 cells (qPCR, n = 3). (e) SLC25A28 protein levels in OE and control cells (Western blot, n = 3). (f) Microglial morphology with/without GSK2795039 (10 μM) treatment; cell body area was quantified (scale bar = 20 μm, n = 3). (g) Mitochondrial iron visualization using Mito‐FerroGreen staining (scale bar = 5 μm). (h) Quantification of mitochondrial iron content by ferrozine assay ( n = 3). (i) CYBB mRNA expression in OE cells with or without GSK2795039 treatment (qPCR, n = 3). (j) NOX2 protein expression in OE cells with or without GSK2795039 treatment (Western blot, n = 3). (k) ROS levels in OE cells with or without GSK2795039 treatment, measured by DCFH‐DA staining (scale bar = 20 μm, n = 6). (l) Expression of inflammatory markers (iNOS, total caspase‐1, and cleaved caspase‐1) in OE cells with or without GSK2795039 treatment (Western blot, n = 3). (m) ELISA quantification of IL‐1β and TNF‐α in OE cells with or without GSK2795039 treatment ( n = 3). Data are expressed as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

Figure Legend Snippet: SLC25A28 regulates microglial activation via NOX2‐dependent ROS pathway. (a) CYBB mRNA levels in SLC25A28‐KO versus control microglia (qPCR, n = 3). (b) NOX2 protein expression in microglia (Western blot, n = 3). (c) Intracellular ROS levels in microglia assessed by DCFH‐DA staining (scale bar = 5 μm, n = 5). (d) SLC25A28 mRNA expression in overexpression (OE) versus control BV2 cells (qPCR, n = 3). (e) SLC25A28 protein levels in OE and control cells (Western blot, n = 3). (f) Microglial morphology with/without GSK2795039 (10 μM) treatment; cell body area was quantified (scale bar = 20 μm, n = 3). (g) Mitochondrial iron visualization using Mito‐FerroGreen staining (scale bar = 5 μm). (h) Quantification of mitochondrial iron content by ferrozine assay ( n = 3). (i) CYBB mRNA expression in OE cells with or without GSK2795039 treatment (qPCR, n = 3). (j) NOX2 protein expression in OE cells with or without GSK2795039 treatment (Western blot, n = 3). (k) ROS levels in OE cells with or without GSK2795039 treatment, measured by DCFH‐DA staining (scale bar = 20 μm, n = 6). (l) Expression of inflammatory markers (iNOS, total caspase‐1, and cleaved caspase‐1) in OE cells with or without GSK2795039 treatment (Western blot, n = 3). (m) ELISA quantification of IL‐1β and TNF‐α in OE cells with or without GSK2795039 treatment ( n = 3). Data are expressed as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques Used: Activation Assay, Control, Expressing, Western Blot, Staining, Over Expression, Ferrozine Assay, Enzyme-linked Immunosorbent Assay

SLC25A28 overexpression promotes NOX2 activation through enhanced heme biosynthesis. (a) ALAS1 mRNA levels in SLC25A28 overexpression (A28 OE) versus control cells (qPCR, n = 3). (b) ALAS1 protein expression in A28 OE and control cells (Western blot, n = 3). (c) Ferrochelatase (FECH) mRNA levels in A28 OE and control cells (qPCR, n = 3). (d) Ferrochelatase protein expression in A28 OE and control cells (Western blot, n = 3). (e) Cellular heme content in A28 OE cells (Oxalate assay, n = 6). (f) Microglial morphology in A28 OE cells with or without succinylacetone (SA) treatment (scale bar = 20 μm, n = 3). (g) NOX2 mRNA levels in A28 OE cells with or without SA treatment (qPCR, n = 3). (h) NOX2 protein expression in A28 OE cells with or without SA treatment (Western blot, n = 3). (i) ROS production in A28 OE cells with or without SA treatment (DCFH‐DA staining, scale bar = 5 μm, n = 6). (j) Inflammatory marker expression in A28 OE cells with or without SA treatment (iNOS, total caspase‐1, and cleaved caspase‐1; Western blot, n = 3). (k) ELISA quantification of IL‐1β and TNF‐α levels in A28 OE cells with or without SA treatment ( n = 3). Data are expressed as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

Figure Legend Snippet: SLC25A28 overexpression promotes NOX2 activation through enhanced heme biosynthesis. (a) ALAS1 mRNA levels in SLC25A28 overexpression (A28 OE) versus control cells (qPCR, n = 3). (b) ALAS1 protein expression in A28 OE and control cells (Western blot, n = 3). (c) Ferrochelatase (FECH) mRNA levels in A28 OE and control cells (qPCR, n = 3). (d) Ferrochelatase protein expression in A28 OE and control cells (Western blot, n = 3). (e) Cellular heme content in A28 OE cells (Oxalate assay, n = 6). (f) Microglial morphology in A28 OE cells with or without succinylacetone (SA) treatment (scale bar = 20 μm, n = 3). (g) NOX2 mRNA levels in A28 OE cells with or without SA treatment (qPCR, n = 3). (h) NOX2 protein expression in A28 OE cells with or without SA treatment (Western blot, n = 3). (i) ROS production in A28 OE cells with or without SA treatment (DCFH‐DA staining, scale bar = 5 μm, n = 6). (j) Inflammatory marker expression in A28 OE cells with or without SA treatment (iNOS, total caspase‐1, and cleaved caspase‐1; Western blot, n = 3). (k) ELISA quantification of IL‐1β and TNF‐α levels in A28 OE cells with or without SA treatment ( n = 3). Data are expressed as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques Used: Over Expression, Activation Assay, Control, Expressing, Western Blot, Staining, Marker, Enzyme-linked Immunosorbent Assay

SLC25A28 knockout attenuates neuroinflammation through heme‐dependent NOX2 activation. (a) ALAS1 mRNA levels in A28‐KO versus control primary microglia (qPCR, n = 3). (b) ALAS1 protein expression in A28‐KO and control microglia (Western blot, n = 3). (c) FECH mRNA levels in A28‐KO versus control microglia (qPCR, n = 3). (d) FECH protein expression in A28‐KO and control microglia (Western blot, n = 3). (e) Cellular heme content in A28‐KO cells (oxalate assay, n = 6). (f) Microglial morphology in A28‐KO cells with or without 5‐aminolevulinic acid (5‐ALA) treatment (scale bar = 20 μm, n = 3). (g) NOX2 mRNA levels in A28‐KO cells with or without 5‐ALA treatment (qPCR, n = 3). (h) NOX2 protein levels in A28‐KO cells with or without 5‐ALA treatment (Western blot, n = 3). (i) ROS production in A28‐KO cells with or without 5‐ALA treatment (DCFH‐DA staining, scale bar = 5 μm, n = 5). (j) Inflammatory marker expression in A28‐KO cells with or without 5‐ALA treatment (iNOS, total caspase‐1, and cleaved caspase‐1; Western blot, n = 3). (k) ELISA quantification of IL‐1β and TNF‐α secretion in A28‐KO cells with or without 5‐ALA treatment ( n = 3). Data are expressed as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

Figure Legend Snippet: SLC25A28 knockout attenuates neuroinflammation through heme‐dependent NOX2 activation. (a) ALAS1 mRNA levels in A28‐KO versus control primary microglia (qPCR, n = 3). (b) ALAS1 protein expression in A28‐KO and control microglia (Western blot, n = 3). (c) FECH mRNA levels in A28‐KO versus control microglia (qPCR, n = 3). (d) FECH protein expression in A28‐KO and control microglia (Western blot, n = 3). (e) Cellular heme content in A28‐KO cells (oxalate assay, n = 6). (f) Microglial morphology in A28‐KO cells with or without 5‐aminolevulinic acid (5‐ALA) treatment (scale bar = 20 μm, n = 3). (g) NOX2 mRNA levels in A28‐KO cells with or without 5‐ALA treatment (qPCR, n = 3). (h) NOX2 protein levels in A28‐KO cells with or without 5‐ALA treatment (Western blot, n = 3). (i) ROS production in A28‐KO cells with or without 5‐ALA treatment (DCFH‐DA staining, scale bar = 5 μm, n = 5). (j) Inflammatory marker expression in A28‐KO cells with or without 5‐ALA treatment (iNOS, total caspase‐1, and cleaved caspase‐1; Western blot, n = 3). (k) ELISA quantification of IL‐1β and TNF‐α secretion in A28‐KO cells with or without 5‐ALA treatment ( n = 3). Data are expressed as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques Used: Knock-Out, Activation Assay, Control, Expressing, Western Blot, Staining, Marker, Enzyme-linked Immunosorbent Assay

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Journal: CNS Neuroscience & Therapeutics

Article Title: Microglial SLC25A28 Knockout Mitigates Spinal Cord Injury in Mice by Inhibiting Heme Synthesis and Subsequent NOX2 Activation

doi: 10.1111/cns.70638

Figure Lengend Snippet: SLC25A28 regulates microglial activation via NOX2‐dependent ROS pathway. (a) CYBB mRNA levels in SLC25A28‐KO versus control microglia (qPCR, n = 3). (b) NOX2 protein expression in microglia (Western blot, n = 3). (c) Intracellular ROS levels in microglia assessed by DCFH‐DA staining (scale bar = 5 μm, n = 5). (d) SLC25A28 mRNA expression in overexpression (OE) versus control BV2 cells (qPCR, n = 3). (e) SLC25A28 protein levels in OE and control cells (Western blot, n = 3). (f) Microglial morphology with/without GSK2795039 (10 μM) treatment; cell body area was quantified (scale bar = 20 μm, n = 3). (g) Mitochondrial iron visualization using Mito‐FerroGreen staining (scale bar = 5 μm). (h) Quantification of mitochondrial iron content by ferrozine assay ( n = 3). (i) CYBB mRNA expression in OE cells with or without GSK2795039 treatment (qPCR, n = 3). (j) NOX2 protein expression in OE cells with or without GSK2795039 treatment (Western blot, n = 3). (k) ROS levels in OE cells with or without GSK2795039 treatment, measured by DCFH‐DA staining (scale bar = 20 μm, n = 6). (l) Expression of inflammatory markers (iNOS, total caspase‐1, and cleaved caspase‐1) in OE cells with or without GSK2795039 treatment (Western blot, n = 3). (m) ELISA quantification of IL‐1β and TNF‐α in OE cells with or without GSK2795039 treatment ( n = 3). Data are expressed as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Specifically, the NOX2 inhibitor GSK2795039 (10 μM, MedChemExpress, HY‐18950, Monmouth Junction, NJ, USA) was added 1 h prior to LPS stimulation in SLC25A28‐overexpressing BV2 cells to suppress NOX2 activity.

Techniques: Activation Assay, Control, Expressing, Western Blot, Staining, Over Expression, Ferrozine Assay, Enzyme-linked Immunosorbent Assay

Journal: CNS Neuroscience & Therapeutics

Article Title: Microglial SLC25A28 Knockout Mitigates Spinal Cord Injury in Mice by Inhibiting Heme Synthesis and Subsequent NOX2 Activation

doi: 10.1111/cns.70638

Figure Lengend Snippet: SLC25A28 overexpression promotes NOX2 activation through enhanced heme biosynthesis. (a) ALAS1 mRNA levels in SLC25A28 overexpression (A28 OE) versus control cells (qPCR, n = 3). (b) ALAS1 protein expression in A28 OE and control cells (Western blot, n = 3). (c) Ferrochelatase (FECH) mRNA levels in A28 OE and control cells (qPCR, n = 3). (d) Ferrochelatase protein expression in A28 OE and control cells (Western blot, n = 3). (e) Cellular heme content in A28 OE cells (Oxalate assay, n = 6). (f) Microglial morphology in A28 OE cells with or without succinylacetone (SA) treatment (scale bar = 20 μm, n = 3). (g) NOX2 mRNA levels in A28 OE cells with or without SA treatment (qPCR, n = 3). (h) NOX2 protein expression in A28 OE cells with or without SA treatment (Western blot, n = 3). (i) ROS production in A28 OE cells with or without SA treatment (DCFH‐DA staining, scale bar = 5 μm, n = 6). (j) Inflammatory marker expression in A28 OE cells with or without SA treatment (iNOS, total caspase‐1, and cleaved caspase‐1; Western blot, n = 3). (k) ELISA quantification of IL‐1β and TNF‐α levels in A28 OE cells with or without SA treatment ( n = 3). Data are expressed as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Over Expression, Activation Assay, Control, Expressing, Western Blot, Staining, Marker, Enzyme-linked Immunosorbent Assay

Journal: CNS Neuroscience & Therapeutics

Article Title: Microglial SLC25A28 Knockout Mitigates Spinal Cord Injury in Mice by Inhibiting Heme Synthesis and Subsequent NOX2 Activation

doi: 10.1111/cns.70638

Figure Lengend Snippet: SLC25A28 knockout attenuates neuroinflammation through heme‐dependent NOX2 activation. (a) ALAS1 mRNA levels in A28‐KO versus control primary microglia (qPCR, n = 3). (b) ALAS1 protein expression in A28‐KO and control microglia (Western blot, n = 3). (c) FECH mRNA levels in A28‐KO versus control microglia (qPCR, n = 3). (d) FECH protein expression in A28‐KO and control microglia (Western blot, n = 3). (e) Cellular heme content in A28‐KO cells (oxalate assay, n = 6). (f) Microglial morphology in A28‐KO cells with or without 5‐aminolevulinic acid (5‐ALA) treatment (scale bar = 20 μm, n = 3). (g) NOX2 mRNA levels in A28‐KO cells with or without 5‐ALA treatment (qPCR, n = 3). (h) NOX2 protein levels in A28‐KO cells with or without 5‐ALA treatment (Western blot, n = 3). (i) ROS production in A28‐KO cells with or without 5‐ALA treatment (DCFH‐DA staining, scale bar = 5 μm, n = 5). (j) Inflammatory marker expression in A28‐KO cells with or without 5‐ALA treatment (iNOS, total caspase‐1, and cleaved caspase‐1; Western blot, n = 3). (k) ELISA quantification of IL‐1β and TNF‐α secretion in A28‐KO cells with or without 5‐ALA treatment ( n = 3). Data are expressed as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Knock-Out, Activation Assay, Control, Expressing, Western Blot, Staining, Marker, Enzyme-linked Immunosorbent Assay

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