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The effect of ozone exposure on tumor cells was studied by measuring ROS levels in B16F10 melanoma and LL2 lung carcinoma cells. (A) The ROS content was assessed using the ROS-ID Total ROS Detection Kit. Data from the 520 nm fluorescence indicates increased ROS levels. The increase in ROS in (B) B16F10 melanoma and (C) LL2 lung carcinoma cells was observed after three days of treatment with air or ozone, with or without arbutin (1.56 µM). These measurements were performed using the Chekine TM reactive oxygen species detection fluorometric assay. (D) Cell proliferation of B16F10 melanoma and LL2 lung carcinoma was evaluated following three-day ozone exposure, revealing enhanced proliferation in both cell lines. Results are shown as mean ± SD with a sample size of 6; statistical significance is indicated by *P < 0.05, **P < 0.01, and ***P < 0.001. Western blot images display the expression of PCNA <t>and</t> <t>HIF-1α</t> proteins in (E) B16F10 (F) LL2 cells exposed to ozone or air at various time points.
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The effect of ozone exposure on tumor cells was studied by measuring ROS levels in B16F10 melanoma and LL2 lung carcinoma cells. (A) The ROS content was assessed using the ROS-ID Total ROS Detection Kit. Data from the 520 nm fluorescence indicates increased ROS levels. The increase in ROS in (B) B16F10 melanoma and (C) LL2 lung carcinoma cells was observed after three days of treatment with air or ozone, with or without arbutin (1.56 µM). These measurements were performed using the Chekine TM reactive oxygen species detection fluorometric assay. (D) Cell proliferation of B16F10 melanoma and LL2 lung carcinoma was evaluated following three-day ozone exposure, revealing enhanced proliferation in both cell lines. Results are shown as mean ± SD with a sample size of 6; statistical significance is indicated by *P < 0.05, **P < 0.01, and ***P < 0.001. Western blot images display the expression of PCNA <t>and</t> <t>HIF-1α</t> proteins in (E) B16F10 (F) LL2 cells exposed to ozone or air at various time points.
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The effect of ozone exposure on tumor cells was studied by measuring ROS levels in B16F10 melanoma and LL2 lung carcinoma cells. (A) The ROS content was assessed using the ROS-ID Total ROS Detection Kit. Data from the 520 nm fluorescence indicates increased ROS levels. The increase in ROS in (B) B16F10 melanoma and (C) LL2 lung carcinoma cells was observed after three days of treatment with air or ozone, with or without arbutin (1.56 µM). These measurements were performed using the Chekine TM reactive oxygen species detection fluorometric assay. (D) Cell proliferation of B16F10 melanoma and LL2 lung carcinoma was evaluated following three-day ozone exposure, revealing enhanced proliferation in both cell lines. Results are shown as mean ± SD with a sample size of 6; statistical significance is indicated by *P < 0.05, **P < 0.01, and ***P < 0.001. Western blot images display the expression of PCNA <t>and</t> <t>HIF-1α</t> proteins in (E) B16F10 (F) LL2 cells exposed to ozone or air at various time points.
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HTRA1 overexpression affected mitochondrial dysfunction via activation of the <t>HIF-1α</t> pathway. ISO-treated HL-1 cells were transfected with OE-HTRA1 and then co-treated with the HIF-1α inhibitor <t>KC7F2</t> or DMSO vehicle. A WB analysis of HIF-1α protein expression. B-E Mitochondrial mass, mitochondrial ROS level, mitochondrial membrane potential and ATP content were respectively quantified by MitoTracker staining, MitoSOX detection, flow cytometry and kit assay. F-G Seahorse analyzer was used to assess OCR and ECAR profile. Data are presented as mean ± SD from three independent biological replicates ( n = 3). Exact p -values are indicated in the figure
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Image Search Results


The effect of ozone exposure on tumor cells was studied by measuring ROS levels in B16F10 melanoma and LL2 lung carcinoma cells. (A) The ROS content was assessed using the ROS-ID Total ROS Detection Kit. Data from the 520 nm fluorescence indicates increased ROS levels. The increase in ROS in (B) B16F10 melanoma and (C) LL2 lung carcinoma cells was observed after three days of treatment with air or ozone, with or without arbutin (1.56 µM). These measurements were performed using the Chekine TM reactive oxygen species detection fluorometric assay. (D) Cell proliferation of B16F10 melanoma and LL2 lung carcinoma was evaluated following three-day ozone exposure, revealing enhanced proliferation in both cell lines. Results are shown as mean ± SD with a sample size of 6; statistical significance is indicated by *P < 0.05, **P < 0.01, and ***P < 0.001. Western blot images display the expression of PCNA and HIF-1α proteins in (E) B16F10 (F) LL2 cells exposed to ozone or air at various time points.

Journal: American Journal of Cancer Research

Article Title: Reactive oxygen species-dependent regulation of hypoxia-inducible factor 1α/C-X-C motif chemokine receptor 4 signaling promotes ozone-induced cancer metastasis

doi: 10.62347/DKDS6537

Figure Lengend Snippet: The effect of ozone exposure on tumor cells was studied by measuring ROS levels in B16F10 melanoma and LL2 lung carcinoma cells. (A) The ROS content was assessed using the ROS-ID Total ROS Detection Kit. Data from the 520 nm fluorescence indicates increased ROS levels. The increase in ROS in (B) B16F10 melanoma and (C) LL2 lung carcinoma cells was observed after three days of treatment with air or ozone, with or without arbutin (1.56 µM). These measurements were performed using the Chekine TM reactive oxygen species detection fluorometric assay. (D) Cell proliferation of B16F10 melanoma and LL2 lung carcinoma was evaluated following three-day ozone exposure, revealing enhanced proliferation in both cell lines. Results are shown as mean ± SD with a sample size of 6; statistical significance is indicated by *P < 0.05, **P < 0.01, and ***P < 0.001. Western blot images display the expression of PCNA and HIF-1α proteins in (E) B16F10 (F) LL2 cells exposed to ozone or air at various time points.

Article Snippet: The HIF-1α inhibitor (SYP-5) was purchased from MedChemExpress (MedChemExpress LLC, Monmouth Junction, NJ, USA).

Techniques: Fluorescence, Western Blot, Expressing

The effects of ozone on the HIF-1α/CXCR4 pathway and EMT markers in B16F10 and LL2 in vitro models. Western blot images showing levels of HIF-1α, CXCR4, E-cadherin, N-cadherin, MMP-2, and SNAIL proteins. Inset values represent protein expression levels normalized to β-Actin.

Journal: American Journal of Cancer Research

Article Title: Reactive oxygen species-dependent regulation of hypoxia-inducible factor 1α/C-X-C motif chemokine receptor 4 signaling promotes ozone-induced cancer metastasis

doi: 10.62347/DKDS6537

Figure Lengend Snippet: The effects of ozone on the HIF-1α/CXCR4 pathway and EMT markers in B16F10 and LL2 in vitro models. Western blot images showing levels of HIF-1α, CXCR4, E-cadherin, N-cadherin, MMP-2, and SNAIL proteins. Inset values represent protein expression levels normalized to β-Actin.

Article Snippet: The HIF-1α inhibitor (SYP-5) was purchased from MedChemExpress (MedChemExpress LLC, Monmouth Junction, NJ, USA).

Techniques: In Vitro, Western Blot, Expressing

The ROS-related effects of in vitro arbutin application on ozone-exposed EMT depolarization and HIF-1α/CXCR4 pathway downregulation in (A) B16F10 and (B) LL2 cells. Protein expressions of HIF-1α, CXCR4, E-cadherin (E-Cad), N-cadherin (N-Cad), MMP-2, and SNAIL are shown with arbutin-reversal treatment. Inset values indicate protein levels normalized to β-Actin. Each experiment was repeated three times with similar results.

Journal: American Journal of Cancer Research

Article Title: Reactive oxygen species-dependent regulation of hypoxia-inducible factor 1α/C-X-C motif chemokine receptor 4 signaling promotes ozone-induced cancer metastasis

doi: 10.62347/DKDS6537

Figure Lengend Snippet: The ROS-related effects of in vitro arbutin application on ozone-exposed EMT depolarization and HIF-1α/CXCR4 pathway downregulation in (A) B16F10 and (B) LL2 cells. Protein expressions of HIF-1α, CXCR4, E-cadherin (E-Cad), N-cadherin (N-Cad), MMP-2, and SNAIL are shown with arbutin-reversal treatment. Inset values indicate protein levels normalized to β-Actin. Each experiment was repeated three times with similar results.

Article Snippet: The HIF-1α inhibitor (SYP-5) was purchased from MedChemExpress (MedChemExpress LLC, Monmouth Junction, NJ, USA).

Techniques: In Vitro

HTRA1 overexpression affected mitochondrial dysfunction via activation of the HIF-1α pathway. ISO-treated HL-1 cells were transfected with OE-HTRA1 and then co-treated with the HIF-1α inhibitor KC7F2 or DMSO vehicle. A WB analysis of HIF-1α protein expression. B-E Mitochondrial mass, mitochondrial ROS level, mitochondrial membrane potential and ATP content were respectively quantified by MitoTracker staining, MitoSOX detection, flow cytometry and kit assay. F-G Seahorse analyzer was used to assess OCR and ECAR profile. Data are presented as mean ± SD from three independent biological replicates ( n = 3). Exact p -values are indicated in the figure

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: ALYREF stabilizes MZF1 via m5C modification to exacerbate cardiac remodeling and atrial fibrillation in heart failure

doi: 10.1007/s00018-026-06273-3

Figure Lengend Snippet: HTRA1 overexpression affected mitochondrial dysfunction via activation of the HIF-1α pathway. ISO-treated HL-1 cells were transfected with OE-HTRA1 and then co-treated with the HIF-1α inhibitor KC7F2 or DMSO vehicle. A WB analysis of HIF-1α protein expression. B-E Mitochondrial mass, mitochondrial ROS level, mitochondrial membrane potential and ATP content were respectively quantified by MitoTracker staining, MitoSOX detection, flow cytometry and kit assay. F-G Seahorse analyzer was used to assess OCR and ECAR profile. Data are presented as mean ± SD from three independent biological replicates ( n = 3). Exact p -values are indicated in the figure

Article Snippet: Specific rescue experiments were performed by co‐treating ALYREF‐knockdown cells with MZF1 overexpression vectors, and HTRA1‐overexpressing cells with the HIF‐1α inhibitor KC7F2 (#HY-18777, MCE, New Jersey, USA) at a concentration of 20 μM for 24 h. All transfections were carried out prior to ISO stimulation.

Techniques: Over Expression, Activation Assay, Transfection, Expressing, Membrane, Staining, Flow Cytometry

ALYREF knockdown improved cardiac remodeling, dysfunction, and atrial fibrillation susceptibility in HF mice. C57BL/6J mice received tail vein injection of AAV carrying sh-ALYREF or sh-NC two weeks prior to ISO injection to induce HF. (A-B) qRT-PCR and WB analysis of ALYREF, MZF1, and HTRA1 mRNA and protein expression in atrial tissue. (C) IHC staining and quantification of HIF-1α in atrial tissues. (D-E) Plasma levels of inflammatory cytokines were quantified by ELISA. (F) HW/BW ratio assessing ventricular hypertrophy. (G-I) WGA staining and Masson’s trichrome staining were respectively performed to evaluate cardiomyocyte cross-sectional area and cardiac fibrosis. (J) H&E staining of atrial tissue sections demonstrating the changes in histopathological conditions. (K-L) Cardiac function status in mice was assessed through echocardiographic images, as well as quantification of FS. (M) Representative ECG tracings from each group revealing mouse heart rate condition. (N-Q) Atrial fibrillation incidence, number of atrial fibrillation episodes, total atrial fibrillation burden, and ventricular rate during atrial fibrillation episodes were assessed. Data are presented as mean ± SD ( n = 10 per group; n = 6 for atrial fibrillation analyses; n = 3 for molecular analyses). Exact p -values are indicated in the figures

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: ALYREF stabilizes MZF1 via m5C modification to exacerbate cardiac remodeling and atrial fibrillation in heart failure

doi: 10.1007/s00018-026-06273-3

Figure Lengend Snippet: ALYREF knockdown improved cardiac remodeling, dysfunction, and atrial fibrillation susceptibility in HF mice. C57BL/6J mice received tail vein injection of AAV carrying sh-ALYREF or sh-NC two weeks prior to ISO injection to induce HF. (A-B) qRT-PCR and WB analysis of ALYREF, MZF1, and HTRA1 mRNA and protein expression in atrial tissue. (C) IHC staining and quantification of HIF-1α in atrial tissues. (D-E) Plasma levels of inflammatory cytokines were quantified by ELISA. (F) HW/BW ratio assessing ventricular hypertrophy. (G-I) WGA staining and Masson’s trichrome staining were respectively performed to evaluate cardiomyocyte cross-sectional area and cardiac fibrosis. (J) H&E staining of atrial tissue sections demonstrating the changes in histopathological conditions. (K-L) Cardiac function status in mice was assessed through echocardiographic images, as well as quantification of FS. (M) Representative ECG tracings from each group revealing mouse heart rate condition. (N-Q) Atrial fibrillation incidence, number of atrial fibrillation episodes, total atrial fibrillation burden, and ventricular rate during atrial fibrillation episodes were assessed. Data are presented as mean ± SD ( n = 10 per group; n = 6 for atrial fibrillation analyses; n = 3 for molecular analyses). Exact p -values are indicated in the figures

Article Snippet: Specific rescue experiments were performed by co‐treating ALYREF‐knockdown cells with MZF1 overexpression vectors, and HTRA1‐overexpressing cells with the HIF‐1α inhibitor KC7F2 (#HY-18777, MCE, New Jersey, USA) at a concentration of 20 μM for 24 h. All transfections were carried out prior to ISO stimulation.

Techniques: Knockdown, Injection, Quantitative RT-PCR, Expressing, Immunohistochemistry, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Staining