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nqo1 (Proteintech)

Name: nqo1
Brand: Proteintech
Rating: 96 (485 reviews)

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Proteintech nqo1

TA improved mitochondrial oxidative damage. A The death rate of HT22 cells was measured by Hoechst/PI staining in HT22 cells after 24 h of OGD/R induction and TA treatment. Magnification: 10 × , scale bar: 200 μm. B Representative images showing ROS release (DHE staining) and viable cells (Hoechst staining) in HT22 cells following OGD/R with or without TA treatment, × 10, scale bar: 200 μm. Bar chart indicates the rate of PI/Hoechst. *** p < 0.001 versus OGD/R alone group, n = 3. C Representative JC-1 staining images depict MMP in HT22 cells following OGD/R with or without TA treatment. Red fluorescence indicates JC-1 aggregates, while green fluorescence indicates the monomeric form. Magnification: 10 × , scale bar: 200 μm. D HT22 cells underwent OGD/R and TA treatment, followed by incubation with Hoechst reagent and Mito-Tracker ™ Red CMXRos to stain nuclei and mitochondria. Images were acquired using a confocal laser scanning microscope. Magnification: 64 ×, scale bar: 5 μm. E The bar chart indicates the DHE/Hoechst rate of HT22 cells. * p <0.05 and *** p < 0.001 versus OGD/R alone group, n = 3. F After 24 h of OGD/R induction and TA treatment, HT22 cell viability was measured by MTT assay, the result is as shown in the bar chart. * p < 0.05, ** p < 0.01 and *** p < 0.001 , and versus OGD/R group, n = 6. G The bar chart indicates the DHE/Hoechst rate of HT22 cells. *** p < 0.001 versus OGD/R alone group, n = 3. H The bar chart illustrates the ratio of JC-1 aggregates to monomers in HT22 cells. *** p < 0.001 versus OGD/R alone group, n = 3. I The bar chart indicates mitochondrial length of HT22 cells in different group. *** p < 0.001 versus OGD/R alone group, n = 3. J Detection of nuclear Nrf2, HO-1, <t>NQO1,</t> and GCLC antioxidant protein expression by Western blotting. K HT22 cells subjected to OGD/R with or without TA, or TA + ML385 (an Nrf2 inhibitor), Western blotting was used to detect Nrf2 protein expression levels. L – O The bar chart indicates the ratios of nuclear Nrf2/LaminB, HO-1/β-actin, NQO1/GAPDH, GCLC/GAPDH. * p < 0.05, ** p < 0.01 and *** p < 0.001 versus OGD/R alone group. P The bar chart demonstrates that TA treatment enhanced OGD/R-induced nuclear Nrf2 expression, an effect reversed by the Nrf2 inhibitor ML385. *** p < 0.001 versus OGD/R group or OGD/R + TA group

Nqo1, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 485 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/nqo1/product/Proteintech
Average 96 stars, based on 485 article reviews

nqo1 - by Bioz Stars, 2026-02

96/100 stars

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1) Product Images from "Thonningianin A derived from Penthorum chinense Pursh alleviates cerebral ischemia/reperfusion-mediated apoptosis and pyroptosis through the activation of PINK1/Parkin-dependent mitophagy"

Article Title: Thonningianin A derived from Penthorum chinense Pursh alleviates cerebral ischemia/reperfusion-mediated apoptosis and pyroptosis through the activation of PINK1/Parkin-dependent mitophagy

Journal: Chinese Medicine

doi: 10.1186/s13020-025-01247-2

Figure Legend Snippet: TA improved mitochondrial oxidative damage. A The death rate of HT22 cells was measured by Hoechst/PI staining in HT22 cells after 24 h of OGD/R induction and TA treatment. Magnification: 10 × , scale bar: 200 μm. B Representative images showing ROS release (DHE staining) and viable cells (Hoechst staining) in HT22 cells following OGD/R with or without TA treatment, × 10, scale bar: 200 μm. Bar chart indicates the rate of PI/Hoechst. *** p < 0.001 versus OGD/R alone group, n = 3. C Representative JC-1 staining images depict MMP in HT22 cells following OGD/R with or without TA treatment. Red fluorescence indicates JC-1 aggregates, while green fluorescence indicates the monomeric form. Magnification: 10 × , scale bar: 200 μm. D HT22 cells underwent OGD/R and TA treatment, followed by incubation with Hoechst reagent and Mito-Tracker ™ Red CMXRos to stain nuclei and mitochondria. Images were acquired using a confocal laser scanning microscope. Magnification: 64 ×, scale bar: 5 μm. E The bar chart indicates the DHE/Hoechst rate of HT22 cells. * p <0.05 and *** p < 0.001 versus OGD/R alone group, n = 3. F After 24 h of OGD/R induction and TA treatment, HT22 cell viability was measured by MTT assay, the result is as shown in the bar chart. * p < 0.05, ** p < 0.01 and *** p < 0.001 , and versus OGD/R group, n = 6. G The bar chart indicates the DHE/Hoechst rate of HT22 cells. *** p < 0.001 versus OGD/R alone group, n = 3. H The bar chart illustrates the ratio of JC-1 aggregates to monomers in HT22 cells. *** p < 0.001 versus OGD/R alone group, n = 3. I The bar chart indicates mitochondrial length of HT22 cells in different group. *** p < 0.001 versus OGD/R alone group, n = 3. J Detection of nuclear Nrf2, HO-1, NQO1, and GCLC antioxidant protein expression by Western blotting. K HT22 cells subjected to OGD/R with or without TA, or TA + ML385 (an Nrf2 inhibitor), Western blotting was used to detect Nrf2 protein expression levels. L – O The bar chart indicates the ratios of nuclear Nrf2/LaminB, HO-1/β-actin, NQO1/GAPDH, GCLC/GAPDH. * p < 0.05, ** p < 0.01 and *** p < 0.001 versus OGD/R alone group. P The bar chart demonstrates that TA treatment enhanced OGD/R-induced nuclear Nrf2 expression, an effect reversed by the Nrf2 inhibitor ML385. *** p < 0.001 versus OGD/R group or OGD/R + TA group

Techniques Used: Staining, Fluorescence, Incubation, Laser-Scanning Microscopy, MTT Assay, Expressing, Western Blot

Image Search Results

Kynurenine-CKA is a Nrf2-dependent inducer of NQO1. (A) Human ARPE-19 cells were seeded into 96-well plates (10,000 cells/well) and treated 24 h post-seeding with either vehicle [0.1 % MeOH (v/v)] or increasing concentrations of: kynurenine, Kyn-CKA, the deaminated Kyn-CKA derivative Dean-Kyn-CKA, the reduced Kyn-CKA derivative Red-Kyn-CKA, or kynurenic acid (KynA). After 24 h, the specific enzyme activity of NQO1 was quantified in cell lysates. Data are shown as fold change in NQO1 specific enzyme activity relative to vehicle control. Values represent means of 8 biological replicates. Dose-response curves were fitted using a four-parameter logistic (4 PL) model in GraphPad Prism. (B) WT and Nrf2-KO BMDMs were seeded into six-well plates (1 × 10 6 /well), allowed to rest overnight, and then treated for 18 h with vehicle or Kyn-CKA (10 μM or 30 μM). The levels of mRNA for Nqo1 were determined by quantitative RT-PCR after normalization to the housekeeping control, B2m . Bars represent means ± SEM (n = 3 biologically independent replicates per condition), with individual data points shown. ∗, p < 0.05. (C,D) WT, Nrf2-KO and Keap1-KD BMDMs were seeded into six-well plates (1 × 10 6 /well), allowed to rest overnight, and subsequently treated with vehicle or Kyn-CKA (10 μM or 30 μM). Whole-cell lysates were collected after 3 h and 24 h and analysed by immunoblotting for Nrf2 at the 3 h timepoint (C) and for Nrf2, Keap1 and NQO1 at the 24h timepoint (D) , with GAPDH serving as a loading control.

Journal: Redox Biology

Article Title: The electrophilic metabolite of kynurenine, kynurenine-CKA, requires C151 in Keap1 to derepress Nrf2

doi: 10.1016/j.redox.2026.104009

Figure Lengend Snippet: Kynurenine-CKA is a Nrf2-dependent inducer of NQO1. (A) Human ARPE-19 cells were seeded into 96-well plates (10,000 cells/well) and treated 24 h post-seeding with either vehicle [0.1 % MeOH (v/v)] or increasing concentrations of: kynurenine, Kyn-CKA, the deaminated Kyn-CKA derivative Dean-Kyn-CKA, the reduced Kyn-CKA derivative Red-Kyn-CKA, or kynurenic acid (KynA). After 24 h, the specific enzyme activity of NQO1 was quantified in cell lysates. Data are shown as fold change in NQO1 specific enzyme activity relative to vehicle control. Values represent means of 8 biological replicates. Dose-response curves were fitted using a four-parameter logistic (4 PL) model in GraphPad Prism. (B) WT and Nrf2-KO BMDMs were seeded into six-well plates (1 × 10 6 /well), allowed to rest overnight, and then treated for 18 h with vehicle or Kyn-CKA (10 μM or 30 μM). The levels of mRNA for Nqo1 were determined by quantitative RT-PCR after normalization to the housekeeping control, B2m . Bars represent means ± SEM (n = 3 biologically independent replicates per condition), with individual data points shown. ∗, p < 0.05. (C,D) WT, Nrf2-KO and Keap1-KD BMDMs were seeded into six-well plates (1 × 10 6 /well), allowed to rest overnight, and subsequently treated with vehicle or Kyn-CKA (10 μM or 30 μM). Whole-cell lysates were collected after 3 h and 24 h and analysed by immunoblotting for Nrf2 at the 3 h timepoint (C) and for Nrf2, Keap1 and NQO1 at the 24h timepoint (D) , with GAPDH serving as a loading control.

Article Snippet: The TaqManTM Gene Expression Assay IDs (Thermo Fisher, Waltham, MA) were: Mm01253561 (for Nqo1 ); Mm00516005 (for Ho1); Mm01324400 (for Gclm ); Mm00434228 (for IL1b ); Mm00446190 (for IL6 ); Mm00441242 (for Mcp1 ); Mm00443252 (for Tnf ); Mm004405021 (for Nos2 ); Mm00437762 (for B2m ); Mm03024075 (for Hprt1 ); and 4352341E (for Actb ).

Techniques: Activity Assay, Control, Quantitative RT-PCR, Western Blot

Kynurenine is an Nrf2 activator in BMDMs. (A) BMDMs were resuspended, seeded into 96-well plates (100,000 cells/well), and treated 24 h post-seeding with either vehicle [0.1 % DMSO (v/v)] or increasing concentrations of kynurenine, TBE-31, or sulforaphane (SFN). After 48 h, the specific enzyme activity of NQO1 was quantified in cell lysates. Data are shown as fold change in NQO1 specific enzyme activity relative to vehicle control. Values represent means of 8 biological replicates. Dose-response curves were fitted using a four-parameter logistic (4PL) model in GraphPad Prism. (B,C) BMDMs, derived from four WT C57BL/6J mice (M1-M4), were seeded into six-well plates (1 × 10 6 /well), allowed to adhere overnight, and subsequently treated with either vehicle or kynurenine (Kyn, 100 μM or 400 μM) for either 3 h or 24 h. Total cell lysates were prepared and the protein levels of NQO1 (B) were determined by immunoblotting 24 h post-treatment. The protein levels of Nrf2 (C) were determined by immunoblotting 3 h post-treatment. The levels of α-tubulin served as a loading control.

Journal: Redox Biology

Article Title: The electrophilic metabolite of kynurenine, kynurenine-CKA, requires C151 in Keap1 to derepress Nrf2

doi: 10.1016/j.redox.2026.104009

Figure Lengend Snippet: Kynurenine is an Nrf2 activator in BMDMs. (A) BMDMs were resuspended, seeded into 96-well plates (100,000 cells/well), and treated 24 h post-seeding with either vehicle [0.1 % DMSO (v/v)] or increasing concentrations of kynurenine, TBE-31, or sulforaphane (SFN). After 48 h, the specific enzyme activity of NQO1 was quantified in cell lysates. Data are shown as fold change in NQO1 specific enzyme activity relative to vehicle control. Values represent means of 8 biological replicates. Dose-response curves were fitted using a four-parameter logistic (4PL) model in GraphPad Prism. (B,C) BMDMs, derived from four WT C57BL/6J mice (M1-M4), were seeded into six-well plates (1 × 10 6 /well), allowed to adhere overnight, and subsequently treated with either vehicle or kynurenine (Kyn, 100 μM or 400 μM) for either 3 h or 24 h. Total cell lysates were prepared and the protein levels of NQO1 (B) were determined by immunoblotting 24 h post-treatment. The protein levels of Nrf2 (C) were determined by immunoblotting 3 h post-treatment. The levels of α-tubulin served as a loading control.

Techniques: Activity Assay, Control, Derivative Assay, Western Blot

Kynurenine induces Nrf2-driven transcription in BMDMs . WT and Nrf2-KO BMDMs were seeded into six-well plates (1 × 10 6 /well), allowed to adhere overnight, and then treated for 18 h with vehicle or kynurenine (Kyn; 20 μM or 200 μM). The levels of mRNA for Nrf2 (gene name Nfe2l2 ) (A) , Keap1 (B) , and the Nrf2 transcriptional targets Nqo1 (C) , Gclm (D) , Gclc (E) , Slc7a11 (F) , and Slc7a5 (G) were determined by quantitative RT-PCR after normalization to the housekeeping control Rps18 (or B2m for Keap1 ). Bars represent means ± SEM (n = 3 biologically independent replicates per condition), with individual data points shown. ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗, p < 0.001; ∗∗∗∗, p < 0.0001.

Journal: Redox Biology

Article Title: The electrophilic metabolite of kynurenine, kynurenine-CKA, requires C151 in Keap1 to derepress Nrf2

doi: 10.1016/j.redox.2026.104009

Figure Lengend Snippet: Kynurenine induces Nrf2-driven transcription in BMDMs . WT and Nrf2-KO BMDMs were seeded into six-well plates (1 × 10 6 /well), allowed to adhere overnight, and then treated for 18 h with vehicle or kynurenine (Kyn; 20 μM or 200 μM). The levels of mRNA for Nrf2 (gene name Nfe2l2 ) (A) , Keap1 (B) , and the Nrf2 transcriptional targets Nqo1 (C) , Gclm (D) , Gclc (E) , Slc7a11 (F) , and Slc7a5 (G) were determined by quantitative RT-PCR after normalization to the housekeeping control Rps18 (or B2m for Keap1 ). Bars represent means ± SEM (n = 3 biologically independent replicates per condition), with individual data points shown. ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗, p < 0.001; ∗∗∗∗, p < 0.0001.

Techniques: Quantitative RT-PCR, Control

C151 in Keap1 is the primary sensor for Kyn-CKA. (A) MEF cells expressing wild-type Keap1 were seeded into 96-well plates (20,000 cells/well), and treated 24 h post-seeding with either vehicle [0.1 % MeOH (v/v)] or increasing concentrations of kynurenine, Kyn-CKA, the deaminated Kyn-CKA derivative Dean-Kyn-CKA, or the reduced Kyn-CKA derivative Red-Kyn-CKA. After 24 h, the specific enzyme activity of NQO1 was quantified in cell lysates. Data are shown as fold change in NQO1 specific enzyme activity relative to vehicle control. Values represent means of 8 biological replicates. Dose-response curves were fitted using a four-parameter logistic (4 PL) model in GraphPad Prism. (B) NQO1 enzyme activity measured using the same experimental conditions in MEF cells expressing either wild-type Keap1 (WT) or the cysteine mutants of Keap1 indicated in figure. (C) WT or Keap1 mutant MEFs were treated for 3 h with 10 nM TBE-31 (a known Nrf2 activator via C151 in Keap1 used as a control), vehicle [0.1 % MeOH (v/v)], 10 μM Kyn-CKA or 10 μM Dean-Kyn-CKA. Whole-cell lysates were collected and analysed by immunoblotting for Nrf2 and Keap1. β-actin served as a loading control. (D) Wild-type (WT) and Keap1 mutant MEFs (C151S/C151S, C288E/C288E, C226S/C226S, C226S/C613S and C613S/C613S) were treated with vehicle [0.1 % MeOH (v/v)], 10 μM Kyn-CKA or 10 μM Dean-Kyn-CKA for 18 h. The mRNA levels for Nqo1 were quantified by RT-qPCR after normalization to the housekeeping control, Gapdh . Bars show means ± SEM; points denote biological replicates. ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗, p < 0.001; ∗∗∗∗, p < 0.0001.

Journal: Redox Biology

Article Title: The electrophilic metabolite of kynurenine, kynurenine-CKA, requires C151 in Keap1 to derepress Nrf2

doi: 10.1016/j.redox.2026.104009

Figure Lengend Snippet: C151 in Keap1 is the primary sensor for Kyn-CKA. (A) MEF cells expressing wild-type Keap1 were seeded into 96-well plates (20,000 cells/well), and treated 24 h post-seeding with either vehicle [0.1 % MeOH (v/v)] or increasing concentrations of kynurenine, Kyn-CKA, the deaminated Kyn-CKA derivative Dean-Kyn-CKA, or the reduced Kyn-CKA derivative Red-Kyn-CKA. After 24 h, the specific enzyme activity of NQO1 was quantified in cell lysates. Data are shown as fold change in NQO1 specific enzyme activity relative to vehicle control. Values represent means of 8 biological replicates. Dose-response curves were fitted using a four-parameter logistic (4 PL) model in GraphPad Prism. (B) NQO1 enzyme activity measured using the same experimental conditions in MEF cells expressing either wild-type Keap1 (WT) or the cysteine mutants of Keap1 indicated in figure. (C) WT or Keap1 mutant MEFs were treated for 3 h with 10 nM TBE-31 (a known Nrf2 activator via C151 in Keap1 used as a control), vehicle [0.1 % MeOH (v/v)], 10 μM Kyn-CKA or 10 μM Dean-Kyn-CKA. Whole-cell lysates were collected and analysed by immunoblotting for Nrf2 and Keap1. β-actin served as a loading control. (D) Wild-type (WT) and Keap1 mutant MEFs (C151S/C151S, C288E/C288E, C226S/C226S, C226S/C613S and C613S/C613S) were treated with vehicle [0.1 % MeOH (v/v)], 10 μM Kyn-CKA or 10 μM Dean-Kyn-CKA for 18 h. The mRNA levels for Nqo1 were quantified by RT-qPCR after normalization to the housekeeping control, Gapdh . Bars show means ± SEM; points denote biological replicates. ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗, p < 0.001; ∗∗∗∗, p < 0.0001.

Techniques: Expressing, Activity Assay, Control, Mutagenesis, Western Blot, Quantitative RT-PCR

The low-dose anti-inflammatory effects of Kyn-CKA in BMDMs are dependent on Nrf2. (A – B) Treatment with Kyn-CKA (5 h) fails to induce the expression of Nqo1 and Gclm in BMDMs obtained from Nrf2-knockout (Nrf2 −/− ) mice. Data are n = 3, ∗∗∗∗p < 0.0001 by two-way ANOVA and Tukey's post-test. (C – G) Effects of Kyn-CKA on the expression of NF-κB−regulated genes in WT and Nrf2-KO BMDMs following 5 h incubation with LPS (0.5 μg/mL) and the indicated concentrations of Kyn-CKA. Data are n = 6, ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001 by two-way ANOVA and Tukey's post-test. Nrf2 was identified as a significant source of variation for MCP1, IL6, TNFα, Nos2, (p < 0.0001) and IL1β (p < 0.005).

Journal: Redox Biology

Article Title: The electrophilic metabolite of kynurenine, kynurenine-CKA, requires C151 in Keap1 to derepress Nrf2

doi: 10.1016/j.redox.2026.104009

Figure Lengend Snippet: The low-dose anti-inflammatory effects of Kyn-CKA in BMDMs are dependent on Nrf2. (A – B) Treatment with Kyn-CKA (5 h) fails to induce the expression of Nqo1 and Gclm in BMDMs obtained from Nrf2-knockout (Nrf2 −/− ) mice. Data are n = 3, ∗∗∗∗p < 0.0001 by two-way ANOVA and Tukey's post-test. (C – G) Effects of Kyn-CKA on the expression of NF-κB−regulated genes in WT and Nrf2-KO BMDMs following 5 h incubation with LPS (0.5 μg/mL) and the indicated concentrations of Kyn-CKA. Data are n = 6, ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001 by two-way ANOVA and Tukey's post-test. Nrf2 was identified as a significant source of variation for MCP1, IL6, TNFα, Nos2, (p < 0.0001) and IL1β (p < 0.005).

Techniques: Expressing, Knock-Out, Incubation

Journal: Chinese Medicine

doi: 10.1186/s13020-025-01247-2

Figure Lengend Snippet: TA improved mitochondrial oxidative damage. A The death rate of HT22 cells was measured by Hoechst/PI staining in HT22 cells after 24 h of OGD/R induction and TA treatment. Magnification: 10 × , scale bar: 200 μm. B Representative images showing ROS release (DHE staining) and viable cells (Hoechst staining) in HT22 cells following OGD/R with or without TA treatment, × 10, scale bar: 200 μm. Bar chart indicates the rate of PI/Hoechst. *** p < 0.001 versus OGD/R alone group, n = 3. C Representative JC-1 staining images depict MMP in HT22 cells following OGD/R with or without TA treatment. Red fluorescence indicates JC-1 aggregates, while green fluorescence indicates the monomeric form. Magnification: 10 × , scale bar: 200 μm. D HT22 cells underwent OGD/R and TA treatment, followed by incubation with Hoechst reagent and Mito-Tracker ™ Red CMXRos to stain nuclei and mitochondria. Images were acquired using a confocal laser scanning microscope. Magnification: 64 ×, scale bar: 5 μm. E The bar chart indicates the DHE/Hoechst rate of HT22 cells. * p <0.05 and *** p < 0.001 versus OGD/R alone group, n = 3. F After 24 h of OGD/R induction and TA treatment, HT22 cell viability was measured by MTT assay, the result is as shown in the bar chart. * p < 0.05, ** p < 0.01 and *** p < 0.001 , and versus OGD/R group, n = 6. G The bar chart indicates the DHE/Hoechst rate of HT22 cells. *** p < 0.001 versus OGD/R alone group, n = 3. H The bar chart illustrates the ratio of JC-1 aggregates to monomers in HT22 cells. *** p < 0.001 versus OGD/R alone group, n = 3. I The bar chart indicates mitochondrial length of HT22 cells in different group. *** p < 0.001 versus OGD/R alone group, n = 3. J Detection of nuclear Nrf2, HO-1, NQO1, and GCLC antioxidant protein expression by Western blotting. K HT22 cells subjected to OGD/R with or without TA, or TA + ML385 (an Nrf2 inhibitor), Western blotting was used to detect Nrf2 protein expression levels. L – O The bar chart indicates the ratios of nuclear Nrf2/LaminB, HO-1/β-actin, NQO1/GAPDH, GCLC/GAPDH. * p < 0.05, ** p < 0.01 and *** p < 0.001 versus OGD/R alone group. P The bar chart demonstrates that TA treatment enhanced OGD/R-induced nuclear Nrf2 expression, an effect reversed by the Nrf2 inhibitor ML385. *** p < 0.001 versus OGD/R group or OGD/R + TA group

Article Snippet: Antibodies against GSDMD (20770-1-Ap), Caspase-3 (25158-1-Ap), Caspase-9 (10380-1-Ap), NQO1 (11451-1-Ap), GCLC (12601-1-Ap), LC3 (14600-1-Ap), PINK1 (23274-1-Ap), Parkin (14060-1-Ap), Antibody Caspase-1 (22,915-1-ap), GAPDH (6004-1-Ig), β-actin (66009-1-Ig), CoraLite ® Plus 488 goat anti-rabbit IgG (RGAR002), CoraLite ® Plus 594-Goat Anti-Mouse IgG (RGAR002), were purchased from Proteintech Group, Inc (Wuhan, China).

Techniques: Staining, Fluorescence, Incubation, Laser-Scanning Microscopy, MTT Assay, Expressing, Western Blot

Alteration in signaling pathways related to tumor growth and immune evasion in the HFD + LPS group of K19-Wnt1/C2mE mice. ( A ) The 8-OHdG content ( left ) and Nqo1 mRNA/ Gapdh mRNA ratio ( right ) of the tumors (control group [n = 4] vs HFD group [n = 4] vs LPS group [n = 3] vs HFD + LPS group [n = 6]). The data are represented in box plots (x = mean). ∗ P < .05, ∗∗ P < .01. Statistical analysis was conducted via the Tukey‒Kramer test. ( B ) Representative images of western blot analysis of TNF-α, TLR4, PD-L1, p-NFκB p65, NFκB, and GAPDH in tumors. The results represent at least 3 independent experiments. ( C ) The density ratio of each band to GAPDH of Western blot analysis was calculated using Image Lab software (Bio-Rad), and the results are presented as box plots (x = mean). ∗ P < .05, ∗∗ P < .01. Statistical analysis was conducted via the Tukey‒Kramer test. ( D ) The relative gene expression levels of Cxcl9 , Ifng , Tnfa , and Cd274 to Gapdh ( Cxcl9, Ifng, Tnf, Cd274 : control group [n = 4] vs HFD group [n = 4] vs LPS group [n = 3] vs HFD + LPS group [n = 6]). The data are represented in box plots (x = mean). ∗ P < .05, ∗∗ P < .01. Statistical analysis was conducted via the Tukey‒Kramer test. Ctrl, control.

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Metabolic Syndrome Develops Cardia Cancer via Nuclear Factor-E2-related Factor 2-Programmed Death-Ligand 1 Signaling

doi: 10.1016/j.jcmgh.2025.101629

Figure Lengend Snippet: Alteration in signaling pathways related to tumor growth and immune evasion in the HFD + LPS group of K19-Wnt1/C2mE mice. ( A ) The 8-OHdG content ( left ) and Nqo1 mRNA/ Gapdh mRNA ratio ( right ) of the tumors (control group [n = 4] vs HFD group [n = 4] vs LPS group [n = 3] vs HFD + LPS group [n = 6]). The data are represented in box plots (x = mean). ∗ P < .05, ∗∗ P < .01. Statistical analysis was conducted via the Tukey‒Kramer test. ( B ) Representative images of western blot analysis of TNF-α, TLR4, PD-L1, p-NFκB p65, NFκB, and GAPDH in tumors. The results represent at least 3 independent experiments. ( C ) The density ratio of each band to GAPDH of Western blot analysis was calculated using Image Lab software (Bio-Rad), and the results are presented as box plots (x = mean). ∗ P < .05, ∗∗ P < .01. Statistical analysis was conducted via the Tukey‒Kramer test. ( D ) The relative gene expression levels of Cxcl9 , Ifng , Tnfa , and Cd274 to Gapdh ( Cxcl9, Ifng, Tnf, Cd274 : control group [n = 4] vs HFD group [n = 4] vs LPS group [n = 3] vs HFD + LPS group [n = 6]). The data are represented in box plots (x = mean). ∗ P < .05, ∗∗ P < .01. Statistical analysis was conducted via the Tukey‒Kramer test. Ctrl, control.

Article Snippet: Nqo1/NQO1 , Applied Biosystems , Mm01253561_m1, Hs01045993_g1.

Techniques: Protein-Protein interactions, Control, Western Blot, Software, Gene Expression

Decrease in expressions of inflammatory cytokines and PD-L1 in Nrf2 -KO K19-Wnt1/C2mE mice stimulated with HFD + LPS. ( A ) The relative gene expression levels of and the relative gene expression levels of Nqo1 Cxcl9 , Ifng , Tnfa, and Cd274 to Gapdh in the tumors (K19-Wnt1/C2mE mice control group [n = 4] vs K19-Wnt1/C2mE mice HFD + LPS group [n = 4] vs Nrf2 -KO-K19-Wnt1/C2mE mice control group [n = 4] vs Nrf2 -KO-K19-Wnt1/C2mE mice HFD + LPS group [n = 6]). The data are represented in box plots (x = mean). ∗ P < .05, ∗∗ P < .01. Statistical analysis was conducted via the Tukey‒Kramer test. ( B ) Representative photos of western blot analysis of protein expression of TLR4, PD-L1, p-NFκB p65, and NFκB in the tumors. The results represent 4 independent experiments. ( C ) The density ratio of each band to GAPDH of Western blot analysis was calculated using Image Lab software (Bio-Rad), and the results are presented as box plots (x = mean). ∗ P < .05, ∗∗ P < .01. Statistical analysis was conducted via the Tukey‒Kramer test. Ctrl, control.

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Metabolic Syndrome Develops Cardia Cancer via Nuclear Factor-E2-related Factor 2-Programmed Death-Ligand 1 Signaling

doi: 10.1016/j.jcmgh.2025.101629

Figure Lengend Snippet: Decrease in expressions of inflammatory cytokines and PD-L1 in Nrf2 -KO K19-Wnt1/C2mE mice stimulated with HFD + LPS. ( A ) The relative gene expression levels of and the relative gene expression levels of Nqo1 Cxcl9 , Ifng , Tnfa, and Cd274 to Gapdh in the tumors (K19-Wnt1/C2mE mice control group [n = 4] vs K19-Wnt1/C2mE mice HFD + LPS group [n = 4] vs Nrf2 -KO-K19-Wnt1/C2mE mice control group [n = 4] vs Nrf2 -KO-K19-Wnt1/C2mE mice HFD + LPS group [n = 6]). The data are represented in box plots (x = mean). ∗ P < .05, ∗∗ P < .01. Statistical analysis was conducted via the Tukey‒Kramer test. ( B ) Representative photos of western blot analysis of protein expression of TLR4, PD-L1, p-NFκB p65, and NFκB in the tumors. The results represent 4 independent experiments. ( C ) The density ratio of each band to GAPDH of Western blot analysis was calculated using Image Lab software (Bio-Rad), and the results are presented as box plots (x = mean). ∗ P < .05, ∗∗ P < .01. Statistical analysis was conducted via the Tukey‒Kramer test. Ctrl, control.

Article Snippet: Nqo1/NQO1 , Applied Biosystems , Mm01253561_m1, Hs01045993_g1.

Techniques: Gene Expression, Control, Western Blot, Expressing, Software

A role of NRF2 stress response in PD-L1 induction by LPS stimulation in MKN7 cells. ( A ) ROS activity in LPS- or TNF-α-stimulated MKN7 cells (control [n = 7] vs LPS [n = 7] vs TNF-α [n = 7]. The data are represented in box plots (x = mean). ∗ P < .05, ∗∗ P < .01. Statistical analysis was performed via the Tukey‒Kramer test. ( B ) Representative images of Western blot analysis of cytoplasmic ( left upper ) and nuclear ( left lower ) NRF2 protein expression in MKN7 cells stimulated with LPS. The results represent 3 independent experiments. The value of the density ratio of each band to that of b-actin ( right upper ) or histone H3 ( right lower ) was calculated via Image Lab (Bio-Rad), and the data are shown in box plots (x = mean). ∗ P < .05, ∗∗ P < .01. Statistical analysis was conducted via Student’s t- test. ( C ) The relative gene expression levels of Nqo1 ( left ) and Cd274 ( right ) to Gapdh in MKN7 cells stimulated with LPS (control [n = 3] vs LPS [n = 3]). The data are represented in box plots (x = mean). ∗ P < .05, ∗∗ P < .01. Statistical analysis was performed via Student’s t- test. ( D ) The relative gene expression levels of NEF2L2 ( left ), NQO1 ( middle ), and CD274 ( right ) to GAPDH in Nrf2 siRNA-transfected MKN7 cells or control siRNA-transfected cells under LPS stimulation (control siRNA + LPS group [n = 3] vs NRF2 siRNA + LPS group [n = 3]). The data are represented in box plots (x = mean). ∗∗ P < .01. Statistical analysis was performed via Student’s t- test. ( E ) ChIP assay using an anti-NRF2 antibody in MKN7 cells treated with or without E coli LPS. Comparison of NRF2 binding to the CD274 promoter (control [n = 3] vs LPS [n = 3]). The values are represented in box plots (x = mean). ∗∗ P < .01. Statistical analysis was performed via Student’s t- test. Ctrl, control.

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Metabolic Syndrome Develops Cardia Cancer via Nuclear Factor-E2-related Factor 2-Programmed Death-Ligand 1 Signaling

doi: 10.1016/j.jcmgh.2025.101629

Figure Lengend Snippet: A role of NRF2 stress response in PD-L1 induction by LPS stimulation in MKN7 cells. ( A ) ROS activity in LPS- or TNF-α-stimulated MKN7 cells (control [n = 7] vs LPS [n = 7] vs TNF-α [n = 7]. The data are represented in box plots (x = mean). ∗ P < .05, ∗∗ P < .01. Statistical analysis was performed via the Tukey‒Kramer test. ( B ) Representative images of Western blot analysis of cytoplasmic ( left upper ) and nuclear ( left lower ) NRF2 protein expression in MKN7 cells stimulated with LPS. The results represent 3 independent experiments. The value of the density ratio of each band to that of b-actin ( right upper ) or histone H3 ( right lower ) was calculated via Image Lab (Bio-Rad), and the data are shown in box plots (x = mean). ∗ P < .05, ∗∗ P < .01. Statistical analysis was conducted via Student’s t- test. ( C ) The relative gene expression levels of Nqo1 ( left ) and Cd274 ( right ) to Gapdh in MKN7 cells stimulated with LPS (control [n = 3] vs LPS [n = 3]). The data are represented in box plots (x = mean). ∗ P < .05, ∗∗ P < .01. Statistical analysis was performed via Student’s t- test. ( D ) The relative gene expression levels of NEF2L2 ( left ), NQO1 ( middle ), and CD274 ( right ) to GAPDH in Nrf2 siRNA-transfected MKN7 cells or control siRNA-transfected cells under LPS stimulation (control siRNA + LPS group [n = 3] vs NRF2 siRNA + LPS group [n = 3]). The data are represented in box plots (x = mean). ∗∗ P < .01. Statistical analysis was performed via Student’s t- test. ( E ) ChIP assay using an anti-NRF2 antibody in MKN7 cells treated with or without E coli LPS. Comparison of NRF2 binding to the CD274 promoter (control [n = 3] vs LPS [n = 3]). The values are represented in box plots (x = mean). ∗∗ P < .01. Statistical analysis was performed via Student’s t- test. Ctrl, control.

Article Snippet: Nqo1/NQO1 , Applied Biosystems , Mm01253561_m1, Hs01045993_g1.

Techniques: Activity Assay, Control, Western Blot, Expressing, Gene Expression, Transfection, Comparison, Binding Assay

Association among protein expression of NQO1 and PD-L1, and Iba1-positive macrophage infiltration in tumor stroma in IHC study in patients with GCA with or without MetS. ( A ) Representative immunohistochemical images of Iba1 ( upper ), NQO1 ( middle ), and PD-L1 ( lower ) in patients with GCA with or without MetS. The cytoplasmic expression of Iba1 in stromal inflammatory cells, and that of NQO1 and PD-L1 in tumor cells in the patients with GCA without MetS ( left ) and with MetS ( right ). Bar = 100 μm. ( B ) The numbers of Iba1-positive macrophage infiltration ( left ), the NQO1 index ( middle ), and the PD-L1 index ( right ) in patients with MetS were significantly higher than those without. The data are represented in box plots (n = 10). ∗ P < .05, ∗∗ P < .01. Student’s t -test and Wilcoxon rank-sum test were applied for statistical analysis of the Iba1-positive cells numbers and the NQO1 and PD-L1 index, respectively. ( C ) Spearman‘s correlation analysis demonstrated positive correlations between the PD-L1 index and the degree of macrophage infiltration and between the PD-L1 index and the NQO1 index (Spearman`s rank correlation coefficient (ρ) value: Iba1 vs PD-L1: ρ = 0.54, P = .013; NQO1 vs PD-L1: ρ = 0.76, P = .0001).

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Metabolic Syndrome Develops Cardia Cancer via Nuclear Factor-E2-related Factor 2-Programmed Death-Ligand 1 Signaling

doi: 10.1016/j.jcmgh.2025.101629

Figure Lengend Snippet: Association among protein expression of NQO1 and PD-L1, and Iba1-positive macrophage infiltration in tumor stroma in IHC study in patients with GCA with or without MetS. ( A ) Representative immunohistochemical images of Iba1 ( upper ), NQO1 ( middle ), and PD-L1 ( lower ) in patients with GCA with or without MetS. The cytoplasmic expression of Iba1 in stromal inflammatory cells, and that of NQO1 and PD-L1 in tumor cells in the patients with GCA without MetS ( left ) and with MetS ( right ). Bar = 100 μm. ( B ) The numbers of Iba1-positive macrophage infiltration ( left ), the NQO1 index ( middle ), and the PD-L1 index ( right ) in patients with MetS were significantly higher than those without. The data are represented in box plots (n = 10). ∗ P < .05, ∗∗ P < .01. Student’s t -test and Wilcoxon rank-sum test were applied for statistical analysis of the Iba1-positive cells numbers and the NQO1 and PD-L1 index, respectively. ( C ) Spearman‘s correlation analysis demonstrated positive correlations between the PD-L1 index and the degree of macrophage infiltration and between the PD-L1 index and the NQO1 index (Spearman`s rank correlation coefficient (ρ) value: Iba1 vs PD-L1: ρ = 0.54, P = .013; NQO1 vs PD-L1: ρ = 0.76, P = .0001).

Article Snippet: Nqo1/NQO1 , Applied Biosystems , Mm01253561_m1, Hs01045993_g1.

Techniques: Expressing, Immunohistochemical staining

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