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Epinephrine and/or chlorpromazine eliminate APAP-induced oxidative stress and inflammation and modulate the expression of the thioredoxin system in the liver. ( A ) and ( B ) demonstrate the hepatic levels of Nrf2 and TNF-α, respectively. ( C ), ( D ), and ( E ) show the effect of EP and CPZ on the thioredoxin system <t>(Trx1/TrxR1)</t> ( C ), thioredoxin-related proteins (TrxL1 and TrxIP) ( D ) mRNA and TrxR1 protein ( E ). Bars represent the mean (± SD) of 3 experiments. Means are compared by two-way ANOVA followed by Tukey’s tests. (*): p < 0.05, ** p < 0.01, *** p < 0.0001, **** p < 0.0001, and “ns” is not significant
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Epinephrine and/or chlorpromazine eliminate APAP-induced oxidative stress and inflammation and modulate the expression of the thioredoxin system in the liver. ( A ) and ( B ) demonstrate the hepatic levels of Nrf2 and TNF-α, respectively. ( C ), ( D ), and ( E ) show the effect of EP and CPZ on the thioredoxin system <t>(Trx1/TrxR1)</t> ( C ), thioredoxin-related proteins (TrxL1 and TrxIP) ( D ) mRNA and TrxR1 protein ( E ). Bars represent the mean (± SD) of 3 experiments. Means are compared by two-way ANOVA followed by Tukey’s tests. (*): p < 0.05, ** p < 0.01, *** p < 0.0001, **** p < 0.0001, and “ns” is not significant
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Epinephrine and/or chlorpromazine eliminate APAP-induced oxidative stress and inflammation and modulate the expression of the thioredoxin system in the liver. ( A ) and ( B ) demonstrate the hepatic levels of Nrf2 and TNF-α, respectively. ( C ), ( D ), and ( E ) show the effect of EP and CPZ on the thioredoxin system <t>(Trx1/TrxR1)</t> ( C ), thioredoxin-related proteins (TrxL1 and TrxIP) ( D ) mRNA and TrxR1 protein ( E ). Bars represent the mean (± SD) of 3 experiments. Means are compared by two-way ANOVA followed by Tukey’s tests. (*): p < 0.05, ** p < 0.01, *** p < 0.0001, **** p < 0.0001, and “ns” is not significant
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Epinephrine and/or chlorpromazine eliminate APAP-induced oxidative stress and inflammation and modulate the expression of the thioredoxin system in the liver. ( A ) and ( B ) demonstrate the hepatic levels of Nrf2 and TNF-α, respectively. ( C ), ( D ), and ( E ) show the effect of EP and CPZ on the thioredoxin system <t>(Trx1/TrxR1)</t> ( C ), thioredoxin-related proteins (TrxL1 and TrxIP) ( D ) mRNA and TrxR1 protein ( E ). Bars represent the mean (± SD) of 3 experiments. Means are compared by two-way ANOVA followed by Tukey’s tests. (*): p < 0.05, ** p < 0.01, *** p < 0.0001, **** p < 0.0001, and “ns” is not significant
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Cusabio elisa kits
Epinephrine and/or chlorpromazine eliminate APAP-induced oxidative stress and inflammation and modulate the expression of the thioredoxin system in the liver. ( A ) and ( B ) demonstrate the hepatic levels of Nrf2 and TNF-α, respectively. ( C ), ( D ), and ( E ) show the effect of EP and CPZ on the thioredoxin system <t>(Trx1/TrxR1)</t> ( C ), thioredoxin-related proteins (TrxL1 and TrxIP) ( D ) mRNA and TrxR1 protein ( E ). Bars represent the mean (± SD) of 3 experiments. Means are compared by two-way ANOVA followed by Tukey’s tests. (*): p < 0.05, ** p < 0.01, *** p < 0.0001, **** p < 0.0001, and “ns” is not significant
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Elabscience Biotechnology thioredoxin
Epinephrine and/or chlorpromazine eliminate APAP-induced oxidative stress and inflammation and modulate the expression of the thioredoxin system in the liver. ( A ) and ( B ) demonstrate the hepatic levels of Nrf2 and TNF-α, respectively. ( C ), ( D ), and ( E ) show the effect of EP and CPZ on the thioredoxin system <t>(Trx1/TrxR1)</t> ( C ), thioredoxin-related proteins (TrxL1 and TrxIP) ( D ) mRNA and TrxR1 protein ( E ). Bars represent the mean (± SD) of 3 experiments. Means are compared by two-way ANOVA followed by Tukey’s tests. (*): p < 0.05, ** p < 0.01, *** p < 0.0001, **** p < 0.0001, and “ns” is not significant
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Abbexa Ltd human thioredoxin reductase 3 (txnrd3) elisa kit
(A) Schematic diagram illustrating the workflow of genome wide CRISPR/Cas9 knockout library screening (CRISPR: Clustered Regularly Interspaced Short Palindromic Repeats) of Cas9-MDA-MB-231 cells treated with either DMSO or Erlotinib (IC 25 , 10 µM). Figure was adapted and modified using BioRender. (B) Volcano plot illustrating the differential guides significantly depleted (in blue) or enriched (in red) in Erlotinib-treated MDA-MB-231 cells compared to DMSO-treated control MDA-MB-231 cells. The differential guides were plotted statistical significance (-log 10 p-value) on the y-axis against fold change (log 2 ) on the x-axis. Each point represents a guide, with those above the significance threshold with fold change greater than 2. <t>TXNRD3</t> guides are highlighted. Source data are provided as a supplementary source file. (C) Protein levels of thioredoxin reductase 1 (TrxR1) and thioredoxin reductase 3 (TrxR3) were analyzed by Western blot analysis in parental and Osimertinib-resistant or persister SUM159PT cells. Representative images of three independent Western blot analysis are shown. Vinculin was used as a loading control.
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(A) Schematic diagram illustrating the workflow of genome wide CRISPR/Cas9 knockout library screening (CRISPR: Clustered Regularly Interspaced Short Palindromic Repeats) of Cas9-MDA-MB-231 cells treated with either DMSO or Erlotinib (IC 25 , 10 µM). Figure was adapted and modified using BioRender. (B) Volcano plot illustrating the differential guides significantly depleted (in blue) or enriched (in red) in Erlotinib-treated MDA-MB-231 cells compared to DMSO-treated control MDA-MB-231 cells. The differential guides were plotted statistical significance (-log 10 p-value) on the y-axis against fold change (log 2 ) on the x-axis. Each point represents a guide, with those above the significance threshold with fold change greater than 2. <t>TXNRD3</t> guides are highlighted. Source data are provided as a supplementary source file. (C) Protein levels of thioredoxin reductase 1 (TrxR1) and thioredoxin reductase 3 (TrxR3) were analyzed by Western blot analysis in parental and Osimertinib-resistant or persister SUM159PT cells. Representative images of three independent Western blot analysis are shown. Vinculin was used as a loading control.
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(A) Schematic diagram illustrating the workflow of genome wide CRISPR/Cas9 knockout library screening (CRISPR: Clustered Regularly Interspaced Short Palindromic Repeats) of Cas9-MDA-MB-231 cells treated with either DMSO or Erlotinib (IC 25 , 10 µM). Figure was adapted and modified using BioRender. (B) Volcano plot illustrating the differential guides significantly depleted (in blue) or enriched (in red) in Erlotinib-treated MDA-MB-231 cells compared to DMSO-treated control MDA-MB-231 cells. The differential guides were plotted statistical significance (-log 10 p-value) on the y-axis against fold change (log 2 ) on the x-axis. Each point represents a guide, with those above the significance threshold with fold change greater than 2. <t>TXNRD3</t> guides are highlighted. Source data are provided as a supplementary source file. (C) Protein levels of thioredoxin reductase 1 (TrxR1) and thioredoxin reductase 3 (TrxR3) were analyzed by Western blot analysis in parental and Osimertinib-resistant or persister SUM159PT cells. Representative images of three independent Western blot analysis are shown. Vinculin was used as a loading control.
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Image Search Results


Epinephrine and/or chlorpromazine eliminate APAP-induced oxidative stress and inflammation and modulate the expression of the thioredoxin system in the liver. ( A ) and ( B ) demonstrate the hepatic levels of Nrf2 and TNF-α, respectively. ( C ), ( D ), and ( E ) show the effect of EP and CPZ on the thioredoxin system (Trx1/TrxR1) ( C ), thioredoxin-related proteins (TrxL1 and TrxIP) ( D ) mRNA and TrxR1 protein ( E ). Bars represent the mean (± SD) of 3 experiments. Means are compared by two-way ANOVA followed by Tukey’s tests. (*): p < 0.05, ** p < 0.01, *** p < 0.0001, **** p < 0.0001, and “ns” is not significant

Journal: BMC Pharmacology & Toxicology

Article Title: Epinephrine-mediated sensitization of thioredoxin 1 enhances chlorpromazine protection against acute hepatotoxicity

doi: 10.1186/s40360-026-01225-w

Figure Lengend Snippet: Epinephrine and/or chlorpromazine eliminate APAP-induced oxidative stress and inflammation and modulate the expression of the thioredoxin system in the liver. ( A ) and ( B ) demonstrate the hepatic levels of Nrf2 and TNF-α, respectively. ( C ), ( D ), and ( E ) show the effect of EP and CPZ on the thioredoxin system (Trx1/TrxR1) ( C ), thioredoxin-related proteins (TrxL1 and TrxIP) ( D ) mRNA and TrxR1 protein ( E ). Bars represent the mean (± SD) of 3 experiments. Means are compared by two-way ANOVA followed by Tukey’s tests. (*): p < 0.05, ** p < 0.01, *** p < 0.0001, **** p < 0.0001, and “ns” is not significant

Article Snippet: Reduced Glutathione (GSH) Colorimetric Assay Kit (Cat. No. E-BC-K030-M), Human Nuclear Factor, Erythroid Derived 2, Like 2 (NFE2L2) ELISA Kit (Cat No. E-EL-H1564), Human TrxR1 (Thioredoxin Reductase 1) ELISA Kit (Cat. No. E-EL-H1728), human TNF-α ELISA Kit (Cat. No. E-EL-H0109) were from Elabscience, Houston, Tx, USA.

Techniques: Expressing

Epinephrine and EGCG effect on cell viability, Nrf2, NTF, and TrxR1 expression in hepatoma cells. HepG2 and Huh7 cells were treated with epinephrine ( A ) or EGCG ( B ) for 24 h, after which cell metabolic activity was determined by MTT assay. Epinephrine enhanced cell viability in both HepG2 and Huh7 cells, whereas EGCG reduced cell viability. ( C ), ( D ), and ( E ) show the protein levels of Nrf2, TNF-α, and TrxR1, respectively, assessed in cells treated with EP, EGCG, CPZ, EP/CPZ, or EGCG/CPZ. Bars represent the mean (± SD) of 3 experiments. Groups were compared using ANOVA followed by Tukey’s tests. (*): p < 0.05, ** p < 0.01, (***): p < 0.001, (****): p < 0.0001, and “ns” is not significant

Journal: BMC Pharmacology & Toxicology

Article Title: Epinephrine-mediated sensitization of thioredoxin 1 enhances chlorpromazine protection against acute hepatotoxicity

doi: 10.1186/s40360-026-01225-w

Figure Lengend Snippet: Epinephrine and EGCG effect on cell viability, Nrf2, NTF, and TrxR1 expression in hepatoma cells. HepG2 and Huh7 cells were treated with epinephrine ( A ) or EGCG ( B ) for 24 h, after which cell metabolic activity was determined by MTT assay. Epinephrine enhanced cell viability in both HepG2 and Huh7 cells, whereas EGCG reduced cell viability. ( C ), ( D ), and ( E ) show the protein levels of Nrf2, TNF-α, and TrxR1, respectively, assessed in cells treated with EP, EGCG, CPZ, EP/CPZ, or EGCG/CPZ. Bars represent the mean (± SD) of 3 experiments. Groups were compared using ANOVA followed by Tukey’s tests. (*): p < 0.05, ** p < 0.01, (***): p < 0.001, (****): p < 0.0001, and “ns” is not significant

Article Snippet: Reduced Glutathione (GSH) Colorimetric Assay Kit (Cat. No. E-BC-K030-M), Human Nuclear Factor, Erythroid Derived 2, Like 2 (NFE2L2) ELISA Kit (Cat No. E-EL-H1564), Human TrxR1 (Thioredoxin Reductase 1) ELISA Kit (Cat. No. E-EL-H1728), human TNF-α ELISA Kit (Cat. No. E-EL-H0109) were from Elabscience, Houston, Tx, USA.

Techniques: Expressing, Activity Assay, MTT Assay

Journal: BMC Pharmacology & Toxicology

Article Title: Epinephrine-mediated sensitization of thioredoxin 1 enhances chlorpromazine protection against acute hepatotoxicity

doi: 10.1186/s40360-026-01225-w

Figure Lengend Snippet:

Article Snippet: Reduced Glutathione (GSH) Colorimetric Assay Kit (Cat. No. E-BC-K030-M), Human Nuclear Factor, Erythroid Derived 2, Like 2 (NFE2L2) ELISA Kit (Cat No. E-EL-H1564), Human TrxR1 (Thioredoxin Reductase 1) ELISA Kit (Cat. No. E-EL-H1728), human TNF-α ELISA Kit (Cat. No. E-EL-H0109) were from Elabscience, Houston, Tx, USA.

Techniques:

(A) Schematic diagram illustrating the workflow of genome wide CRISPR/Cas9 knockout library screening (CRISPR: Clustered Regularly Interspaced Short Palindromic Repeats) of Cas9-MDA-MB-231 cells treated with either DMSO or Erlotinib (IC 25 , 10 µM). Figure was adapted and modified using BioRender. (B) Volcano plot illustrating the differential guides significantly depleted (in blue) or enriched (in red) in Erlotinib-treated MDA-MB-231 cells compared to DMSO-treated control MDA-MB-231 cells. The differential guides were plotted statistical significance (-log 10 p-value) on the y-axis against fold change (log 2 ) on the x-axis. Each point represents a guide, with those above the significance threshold with fold change greater than 2. TXNRD3 guides are highlighted. Source data are provided as a supplementary source file. (C) Protein levels of thioredoxin reductase 1 (TrxR1) and thioredoxin reductase 3 (TrxR3) were analyzed by Western blot analysis in parental and Osimertinib-resistant or persister SUM159PT cells. Representative images of three independent Western blot analysis are shown. Vinculin was used as a loading control.

Journal: bioRxiv

Article Title: Thioredoxin reductase 3 inhibition sensitizes triple-negative breast cancer cells to EGFR inhibitors

doi: 10.1101/2025.03.16.642742

Figure Lengend Snippet: (A) Schematic diagram illustrating the workflow of genome wide CRISPR/Cas9 knockout library screening (CRISPR: Clustered Regularly Interspaced Short Palindromic Repeats) of Cas9-MDA-MB-231 cells treated with either DMSO or Erlotinib (IC 25 , 10 µM). Figure was adapted and modified using BioRender. (B) Volcano plot illustrating the differential guides significantly depleted (in blue) or enriched (in red) in Erlotinib-treated MDA-MB-231 cells compared to DMSO-treated control MDA-MB-231 cells. The differential guides were plotted statistical significance (-log 10 p-value) on the y-axis against fold change (log 2 ) on the x-axis. Each point represents a guide, with those above the significance threshold with fold change greater than 2. TXNRD3 guides are highlighted. Source data are provided as a supplementary source file. (C) Protein levels of thioredoxin reductase 1 (TrxR1) and thioredoxin reductase 3 (TrxR3) were analyzed by Western blot analysis in parental and Osimertinib-resistant or persister SUM159PT cells. Representative images of three independent Western blot analysis are shown. Vinculin was used as a loading control.

Article Snippet: TXNRD3 levels were analyzed in the protein lysates using Human Thioredoxin Reductase 3 (TXNRD3) ELISA Kit (abx384053, Abbexa, UK) as per the manufacturer’s instructions.

Techniques: Genome Wide, CRISPR, Knock-Out, Library Screening, Modification, Control, Western Blot

(A) SUM159PT cells were transfected either with scramble or control siRNA, TrxR1-specific siRNA, or TrxR3-specific siRNA for 48 hours. TrxR1 and TrxR3 mRNA levels were analyzed by RT-qPCR analysis. One-way ANOVA followed by Tukey’s post-test, n = 3 (mean ± SEM). (B) SUM159PT cells were transfected with either scramble or control siRNAs, TrxR1-specific siRNAs, or TrxR3-specific siRNAs for 24 hours and subsequently treated with Erlotinib (0-50 µM) or Osimertinib (0-10 µM) for 72 hours. Cell viability was analyzed by MT cell viability assays. One-way ANOVA followed by Tukey’s post-test, n = 3 (mean ± SEM). (C) MDA-MB-231 cells were transfected either with scramble or control siRNA, TrxR1-specific siRNA, or TrxR3-specific siRNA for 48 hours. TrxR1 and TrxR3 protein levels were analyzed by Western blot analysis. Representative images of three independent experiments are shown. GAPDH was used as a loading control. (D) MDA-MB-231 cells were transfected with either scramble or control siRNAs, TrxR1-specific siRNAs, or TrxR3-specific siRNAs for 24 hours and subsequently treated with Erlotinib (0-50 µM) or Osimertinib (0-10 µM) for 72 hours. Cell viability was analyzed by MT cell viability assays. One-way ANOVA followed by Tukey’s post-test, n = 3 (mean ± SEM). (E) SUM159PT and MDA-MB-231 cells were treated with Auranofin (0-2.5 µM) for 24 hours. Intracellular levels of TXNRD3 were analysed by ELISA assays. One-way ANOVA followed by Tukey’s post-test, n = 3 (mean ± SEM).

Journal: bioRxiv

Article Title: Thioredoxin reductase 3 inhibition sensitizes triple-negative breast cancer cells to EGFR inhibitors

doi: 10.1101/2025.03.16.642742

Figure Lengend Snippet: (A) SUM159PT cells were transfected either with scramble or control siRNA, TrxR1-specific siRNA, or TrxR3-specific siRNA for 48 hours. TrxR1 and TrxR3 mRNA levels were analyzed by RT-qPCR analysis. One-way ANOVA followed by Tukey’s post-test, n = 3 (mean ± SEM). (B) SUM159PT cells were transfected with either scramble or control siRNAs, TrxR1-specific siRNAs, or TrxR3-specific siRNAs for 24 hours and subsequently treated with Erlotinib (0-50 µM) or Osimertinib (0-10 µM) for 72 hours. Cell viability was analyzed by MT cell viability assays. One-way ANOVA followed by Tukey’s post-test, n = 3 (mean ± SEM). (C) MDA-MB-231 cells were transfected either with scramble or control siRNA, TrxR1-specific siRNA, or TrxR3-specific siRNA for 48 hours. TrxR1 and TrxR3 protein levels were analyzed by Western blot analysis. Representative images of three independent experiments are shown. GAPDH was used as a loading control. (D) MDA-MB-231 cells were transfected with either scramble or control siRNAs, TrxR1-specific siRNAs, or TrxR3-specific siRNAs for 24 hours and subsequently treated with Erlotinib (0-50 µM) or Osimertinib (0-10 µM) for 72 hours. Cell viability was analyzed by MT cell viability assays. One-way ANOVA followed by Tukey’s post-test, n = 3 (mean ± SEM). (E) SUM159PT and MDA-MB-231 cells were treated with Auranofin (0-2.5 µM) for 24 hours. Intracellular levels of TXNRD3 were analysed by ELISA assays. One-way ANOVA followed by Tukey’s post-test, n = 3 (mean ± SEM).

Article Snippet: TXNRD3 levels were analyzed in the protein lysates using Human Thioredoxin Reductase 3 (TXNRD3) ELISA Kit (abx384053, Abbexa, UK) as per the manufacturer’s instructions.

Techniques: Transfection, Control, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay