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mitosox red fluorescent probe  (MedChemExpress)


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    MedChemExpress mitosox red fluorescent probe
    Conditional knockout of ZnT3 inhibited the phosphorylation of STAT3 in induced mitochondrial apoptosis in cerebral ischemia/reperfusion mice. (A, B) Western blot analysis of p‐STAT3 expression in isolated mitochondria from ZnT3‐cKO or control mice after 60‐min ischemia followed by 24‐h reperfusion ( n = 6 per group). (C) Representative JC‐1 red fluorescence images showing mitochondrial membrane potential in mitochondria isolated from ischemic hemisphere. Scale bar: 100 μm. (D) Quantification of JC‐1 red/green fluorescence ratio in mitochondria isolated from ischemic hemisphere ( n = 3 per group). (E) Quantitative analysis of mitochondrial ROS levels assessed by <t>MitoSOX</t> staining ( n = 3 per group). (F, G) Western blot analysis of Cytochrome C (Cyt C) expression in brain mitochondria from ZnT3‐cKO or control mice with or without ZnCl 2 treatment ( n = 6 per group). Data were presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus Control + Saline; #### p < 0.0001 versus cKO + Saline.
    Mitosox Red Fluorescent Probe, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 339 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mitosox red fluorescent probe/product/MedChemExpress
    Average 97 stars, based on 339 article reviews
    mitosox red fluorescent probe - by Bioz Stars, 2026-05
    97/100 stars

    Images

    1) Product Images from "Zinc Overload in Microvessels Contributes to Blood–Brain Barrier Disruption by Activating the JAK2 Pathway After Cerebral Ischemia/Reperfusion"

    Article Title: Zinc Overload in Microvessels Contributes to Blood–Brain Barrier Disruption by Activating the JAK2 Pathway After Cerebral Ischemia/Reperfusion

    Journal: CNS Neuroscience & Therapeutics

    doi: 10.1002/cns.70885

    Conditional knockout of ZnT3 inhibited the phosphorylation of STAT3 in induced mitochondrial apoptosis in cerebral ischemia/reperfusion mice. (A, B) Western blot analysis of p‐STAT3 expression in isolated mitochondria from ZnT3‐cKO or control mice after 60‐min ischemia followed by 24‐h reperfusion ( n = 6 per group). (C) Representative JC‐1 red fluorescence images showing mitochondrial membrane potential in mitochondria isolated from ischemic hemisphere. Scale bar: 100 μm. (D) Quantification of JC‐1 red/green fluorescence ratio in mitochondria isolated from ischemic hemisphere ( n = 3 per group). (E) Quantitative analysis of mitochondrial ROS levels assessed by MitoSOX staining ( n = 3 per group). (F, G) Western blot analysis of Cytochrome C (Cyt C) expression in brain mitochondria from ZnT3‐cKO or control mice with or without ZnCl 2 treatment ( n = 6 per group). Data were presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus Control + Saline; #### p < 0.0001 versus cKO + Saline.
    Figure Legend Snippet: Conditional knockout of ZnT3 inhibited the phosphorylation of STAT3 in induced mitochondrial apoptosis in cerebral ischemia/reperfusion mice. (A, B) Western blot analysis of p‐STAT3 expression in isolated mitochondria from ZnT3‐cKO or control mice after 60‐min ischemia followed by 24‐h reperfusion ( n = 6 per group). (C) Representative JC‐1 red fluorescence images showing mitochondrial membrane potential in mitochondria isolated from ischemic hemisphere. Scale bar: 100 μm. (D) Quantification of JC‐1 red/green fluorescence ratio in mitochondria isolated from ischemic hemisphere ( n = 3 per group). (E) Quantitative analysis of mitochondrial ROS levels assessed by MitoSOX staining ( n = 3 per group). (F, G) Western blot analysis of Cytochrome C (Cyt C) expression in brain mitochondria from ZnT3‐cKO or control mice with or without ZnCl 2 treatment ( n = 6 per group). Data were presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus Control + Saline; #### p < 0.0001 versus cKO + Saline.

    Techniques Used: Knock-Out, Phospho-proteomics, Western Blot, Expressing, Isolation, Control, Fluorescence, Membrane, Staining, Saline



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    Conditional knockout of ZnT3 inhibited the phosphorylation of STAT3 in induced mitochondrial apoptosis in cerebral ischemia/reperfusion mice. (A, B) Western blot analysis of p‐STAT3 expression in isolated mitochondria from ZnT3‐cKO or control mice after 60‐min ischemia followed by 24‐h reperfusion ( n = 6 per group). (C) Representative JC‐1 red fluorescence images showing mitochondrial membrane potential in mitochondria isolated from ischemic hemisphere. Scale bar: 100 μm. (D) Quantification of JC‐1 red/green fluorescence ratio in mitochondria isolated from ischemic hemisphere ( n = 3 per group). (E) Quantitative analysis of mitochondrial ROS levels assessed by <t>MitoSOX</t> staining ( n = 3 per group). (F, G) Western blot analysis of Cytochrome C (Cyt C) expression in brain mitochondria from ZnT3‐cKO or control mice with or without ZnCl 2 treatment ( n = 6 per group). Data were presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus Control + Saline; #### p < 0.0001 versus cKO + Saline.
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    Image Search Results


    Conditional knockout of ZnT3 inhibited the phosphorylation of STAT3 in induced mitochondrial apoptosis in cerebral ischemia/reperfusion mice. (A, B) Western blot analysis of p‐STAT3 expression in isolated mitochondria from ZnT3‐cKO or control mice after 60‐min ischemia followed by 24‐h reperfusion ( n = 6 per group). (C) Representative JC‐1 red fluorescence images showing mitochondrial membrane potential in mitochondria isolated from ischemic hemisphere. Scale bar: 100 μm. (D) Quantification of JC‐1 red/green fluorescence ratio in mitochondria isolated from ischemic hemisphere ( n = 3 per group). (E) Quantitative analysis of mitochondrial ROS levels assessed by MitoSOX staining ( n = 3 per group). (F, G) Western blot analysis of Cytochrome C (Cyt C) expression in brain mitochondria from ZnT3‐cKO or control mice with or without ZnCl 2 treatment ( n = 6 per group). Data were presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus Control + Saline; #### p < 0.0001 versus cKO + Saline.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: Zinc Overload in Microvessels Contributes to Blood–Brain Barrier Disruption by Activating the JAK2 Pathway After Cerebral Ischemia/Reperfusion

    doi: 10.1002/cns.70885

    Figure Lengend Snippet: Conditional knockout of ZnT3 inhibited the phosphorylation of STAT3 in induced mitochondrial apoptosis in cerebral ischemia/reperfusion mice. (A, B) Western blot analysis of p‐STAT3 expression in isolated mitochondria from ZnT3‐cKO or control mice after 60‐min ischemia followed by 24‐h reperfusion ( n = 6 per group). (C) Representative JC‐1 red fluorescence images showing mitochondrial membrane potential in mitochondria isolated from ischemic hemisphere. Scale bar: 100 μm. (D) Quantification of JC‐1 red/green fluorescence ratio in mitochondria isolated from ischemic hemisphere ( n = 3 per group). (E) Quantitative analysis of mitochondrial ROS levels assessed by MitoSOX staining ( n = 3 per group). (F, G) Western blot analysis of Cytochrome C (Cyt C) expression in brain mitochondria from ZnT3‐cKO or control mice with or without ZnCl 2 treatment ( n = 6 per group). Data were presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus Control + Saline; #### p < 0.0001 versus cKO + Saline.

    Article Snippet: Mitochondrial superoxide levels were detected using the MitoSOX Red fluorescent probe (MedChemExpress) [ ].

    Techniques: Knock-Out, Phospho-proteomics, Western Blot, Expressing, Isolation, Control, Fluorescence, Membrane, Staining, Saline