rosiglitazone Search Results


99
MedChemExpress rosiglitazone
The PPARγ-HK2 pathway promotes the efferocytosis of LPMs against ferroptotic THP-1 cells. ( A ) The mRNA expression level of PPARγ in LPMs incubated with nontreated or Erastin-treated THP-1 cells for 4 h (normalised to β-actin). ( B ) Cell viability of LPMs treated with 10 µM PPARγ agonist, <t>Rosiglitazone</t> or 10 µM PPARγ inhibitor, T0070907 for 18 h. ( C , D ) LPMs treated as above were incubated with nontreated or Erastin-treated THP-1 cells for 4 h. Efferocytosis of LPMs from each group was determined by ( C ) flow cytometry and ( D ) confocal microscope (scale bar: 50 μm). ( E ) The mRNA expression level of HK2 in LPMs treated as above was detected by qRT-PCR. ( F , G ) qRT-PCR analysis ( F ) and Western blotting ( G ) showed the mRNA and protein levels of HK2 in LPMs transfected with three interfering fragments of HK2 (si-HK2) for 24 h. Full-length blots are presented in Supplementary Fig. 6. ( H , I ) LPMs were transfected with siHK2 for 24 h before stimulated with 10 µM Rosiglitazone, then incubated with Erastin-treated THP-1 cells stained by CFSE for 4 h. Efferocytosis of LPMs from each group was determined by ( H ) flow cytometry and ( I ) confocal microscope (scale bar: 40 μm). Values are mean ± SD. * p < 0.05, ** p < 0.01, ns denotes p > 0.05 (by unpaired Student’s t test).
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94
Tocris rosiglitazone
A, B Bar chart with individual points showing the mRNA expression levels of Il6 and Cox2 in control (vehicle, DMSO) and/or GPR109A‐silenced C2C12 myoblasts exposed to LPS (1 μg/ml) in the presence or absence of either MK1903 (1 μM), <t>rosiglitazone</t> (1 μM), or T007 (1 μM). C Time‐dependent effect of NaB (3 mM), MK1903 (1 μM), and rosiglitazone (1 μM) on autophagosome formation measured in C2C12 myoblasts. Data are expressed as fluorescence intensity normalized to controls (%). Data Information: Each bar is the mean ± S.E.M. of at least 3 independent replicates. * P ≤ 0.05 vs. the veh group. ± P ≤ 0.05 vs. the LPS group; # P ≤ 0.05 vs. the other experimental groups (A) or the veh group (B) calculated using ANOVA.
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86
ChemAxon LLC drug rosiglitazone
Main physico-chemical descriptors of the investigated drugs molecular properties.
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Santa Cruz Biotechnology rosiglitazone
Main physico-chemical descriptors of the investigated drugs molecular properties.
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Selleck Chemicals rosiglitazone
Main physico-chemical descriptors of the investigated drugs molecular properties.
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Toronto Research Chemicals rosiglitazone
Main physico-chemical descriptors of the investigated drugs molecular properties.
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LKT Laboratories sulforaphane sfn
Main physico-chemical descriptors of the investigated drugs molecular properties.
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Selleck Chemicals intracellular ros levels
Cisplatin increases <t>intracellular</t> reactive oxygen species <t>(ROS)</t> levels. Cytosolic ROS ( A ) and mitochondrial superoxide ( B ) levels in PEA1 and PEA2 cells treated with cisplatin at indicated concentrations for 24 h were quantified by flow cytometry using H 2 DCFDA dye and MitoSOX, respectively. Data are represented as mean fluorescence intensity and expressed as mean ± S.E.M. from three independent experiments. Significance was assessed by two-tailed Student’s t -test (* p -value < 0.05, ns p -value > 0.05). Representative histograms of H 2 DCFDA and MitoSOX expression are shown in the overlay.
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TargetMol t0334
Cisplatin increases <t>intracellular</t> reactive oxygen species <t>(ROS)</t> levels. Cytosolic ROS ( A ) and mitochondrial superoxide ( B ) levels in PEA1 and PEA2 cells treated with cisplatin at indicated concentrations for 24 h were quantified by flow cytometry using H 2 DCFDA dye and MitoSOX, respectively. Data are represented as mean fluorescence intensity and expressed as mean ± S.E.M. from three independent experiments. Significance was assessed by two-tailed Student’s t -test (* p -value < 0.05, ns p -value > 0.05). Representative histograms of H 2 DCFDA and MitoSOX expression are shown in the overlay.
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European Directorate for the Quality of Medicines and HealthCare metformin hydrochloride
Fig. 2. Representative chromatogram of a standard mixture solution of <t>Metformin</t> <t>hydrochloride,</t>
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Image Search Results


The PPARγ-HK2 pathway promotes the efferocytosis of LPMs against ferroptotic THP-1 cells. ( A ) The mRNA expression level of PPARγ in LPMs incubated with nontreated or Erastin-treated THP-1 cells for 4 h (normalised to β-actin). ( B ) Cell viability of LPMs treated with 10 µM PPARγ agonist, Rosiglitazone or 10 µM PPARγ inhibitor, T0070907 for 18 h. ( C , D ) LPMs treated as above were incubated with nontreated or Erastin-treated THP-1 cells for 4 h. Efferocytosis of LPMs from each group was determined by ( C ) flow cytometry and ( D ) confocal microscope (scale bar: 50 μm). ( E ) The mRNA expression level of HK2 in LPMs treated as above was detected by qRT-PCR. ( F , G ) qRT-PCR analysis ( F ) and Western blotting ( G ) showed the mRNA and protein levels of HK2 in LPMs transfected with three interfering fragments of HK2 (si-HK2) for 24 h. Full-length blots are presented in Supplementary Fig. 6. ( H , I ) LPMs were transfected with siHK2 for 24 h before stimulated with 10 µM Rosiglitazone, then incubated with Erastin-treated THP-1 cells stained by CFSE for 4 h. Efferocytosis of LPMs from each group was determined by ( H ) flow cytometry and ( I ) confocal microscope (scale bar: 40 μm). Values are mean ± SD. * p < 0.05, ** p < 0.01, ns denotes p > 0.05 (by unpaired Student’s t test).

Journal: Stem Cell Research & Therapy

Article Title: MSCs promote the efferocytosis of large peritoneal macrophages to eliminate ferroptotic monocytes/macrophages in the injured endometria

doi: 10.1186/s13287-024-03742-z

Figure Lengend Snippet: The PPARγ-HK2 pathway promotes the efferocytosis of LPMs against ferroptotic THP-1 cells. ( A ) The mRNA expression level of PPARγ in LPMs incubated with nontreated or Erastin-treated THP-1 cells for 4 h (normalised to β-actin). ( B ) Cell viability of LPMs treated with 10 µM PPARγ agonist, Rosiglitazone or 10 µM PPARγ inhibitor, T0070907 for 18 h. ( C , D ) LPMs treated as above were incubated with nontreated or Erastin-treated THP-1 cells for 4 h. Efferocytosis of LPMs from each group was determined by ( C ) flow cytometry and ( D ) confocal microscope (scale bar: 50 μm). ( E ) The mRNA expression level of HK2 in LPMs treated as above was detected by qRT-PCR. ( F , G ) qRT-PCR analysis ( F ) and Western blotting ( G ) showed the mRNA and protein levels of HK2 in LPMs transfected with three interfering fragments of HK2 (si-HK2) for 24 h. Full-length blots are presented in Supplementary Fig. 6. ( H , I ) LPMs were transfected with siHK2 for 24 h before stimulated with 10 µM Rosiglitazone, then incubated with Erastin-treated THP-1 cells stained by CFSE for 4 h. Efferocytosis of LPMs from each group was determined by ( H ) flow cytometry and ( I ) confocal microscope (scale bar: 40 μm). Values are mean ± SD. * p < 0.05, ** p < 0.01, ns denotes p > 0.05 (by unpaired Student’s t test).

Article Snippet: Erastin (Catalog # HY-15,763), Cytochalasin D (Catalog # HY-N6682), 2-Deoxy-D-glucose (Catalog # HY-13,966), Rosiglitazone (Catalog # HY-17,386), T0070907 (Catalog # HY-13,202), and Bafilomycin A1 (Catalog # HY-100,558) were purchased from MedChem Express (Monmouth Junction, NJ, USA).

Techniques: Expressing, Incubation, Flow Cytometry, Microscopy, Quantitative RT-PCR, Western Blot, Transfection, Staining

A, B Bar chart with individual points showing the mRNA expression levels of Il6 and Cox2 in control (vehicle, DMSO) and/or GPR109A‐silenced C2C12 myoblasts exposed to LPS (1 μg/ml) in the presence or absence of either MK1903 (1 μM), rosiglitazone (1 μM), or T007 (1 μM). C Time‐dependent effect of NaB (3 mM), MK1903 (1 μM), and rosiglitazone (1 μM) on autophagosome formation measured in C2C12 myoblasts. Data are expressed as fluorescence intensity normalized to controls (%). Data Information: Each bar is the mean ± S.E.M. of at least 3 independent replicates. * P ≤ 0.05 vs. the veh group. ± P ≤ 0.05 vs. the LPS group; # P ≤ 0.05 vs. the other experimental groups (A) or the veh group (B) calculated using ANOVA.

Journal: EMBO Molecular Medicine

Article Title: Targeting gut dysbiosis against inflammation and impaired autophagy in Duchenne muscular dystrophy

doi: 10.15252/emmm.202216225

Figure Lengend Snippet: A, B Bar chart with individual points showing the mRNA expression levels of Il6 and Cox2 in control (vehicle, DMSO) and/or GPR109A‐silenced C2C12 myoblasts exposed to LPS (1 μg/ml) in the presence or absence of either MK1903 (1 μM), rosiglitazone (1 μM), or T007 (1 μM). C Time‐dependent effect of NaB (3 mM), MK1903 (1 μM), and rosiglitazone (1 μM) on autophagosome formation measured in C2C12 myoblasts. Data are expressed as fluorescence intensity normalized to controls (%). Data Information: Each bar is the mean ± S.E.M. of at least 3 independent replicates. * P ≤ 0.05 vs. the veh group. ± P ≤ 0.05 vs. the LPS group; # P ≤ 0.05 vs. the other experimental groups (A) or the veh group (B) calculated using ANOVA.

Article Snippet: Primary myoblasts were differentiated in myotubes using a commercially available skeletal muscle differentiation medium (Cat# C‐23061, PromoCell, USA) provided by VWR International PBI S.r.l. in the presence or not of NaB 3 mM (Cat# 303410 Life Technologies), MK1903 (Cat# 4622, Tocris UK), or rosiglitazone (Cat# 5325, Tocris UK).

Techniques: Expressing, Control, Fluorescence

A–F Bar chart with individual points showing the mRNA expression levels of Cb1 , Daglα , Daglβ , Magl , Napepld , and Faah in control (vehicle, DMSO) and/or GPR109A‐silenced C2C12 myoblasts exposed to LPS (1 μg/ml) in the presence or absence of either MK1903 (1 μM), rosiglitazone (1 μM), or T007 (1 μM). G, H Levels of AEA and 2‐AG were measured in C2C12 cells exposed to LPS (1 μg/ml) or NaB (3 mM) for 24 h. I Effect of ACEA (1 μM) and rimonabant (1 μM) on autophagosome formation measured in C2C12 cells. Data Information: Each bar is the mean ± S.E.M. from 3 independent biological replicates. ** P ≤ 0.005; * P ≤ 0.05 vs. the veh group; ± P ≤ 0.05 vs. the LPS group calculated using ANOVA.

Journal: EMBO Molecular Medicine

Article Title: Targeting gut dysbiosis against inflammation and impaired autophagy in Duchenne muscular dystrophy

doi: 10.15252/emmm.202216225

Figure Lengend Snippet: A–F Bar chart with individual points showing the mRNA expression levels of Cb1 , Daglα , Daglβ , Magl , Napepld , and Faah in control (vehicle, DMSO) and/or GPR109A‐silenced C2C12 myoblasts exposed to LPS (1 μg/ml) in the presence or absence of either MK1903 (1 μM), rosiglitazone (1 μM), or T007 (1 μM). G, H Levels of AEA and 2‐AG were measured in C2C12 cells exposed to LPS (1 μg/ml) or NaB (3 mM) for 24 h. I Effect of ACEA (1 μM) and rimonabant (1 μM) on autophagosome formation measured in C2C12 cells. Data Information: Each bar is the mean ± S.E.M. from 3 independent biological replicates. ** P ≤ 0.005; * P ≤ 0.05 vs. the veh group; ± P ≤ 0.05 vs. the LPS group calculated using ANOVA.

Article Snippet: Primary myoblasts were differentiated in myotubes using a commercially available skeletal muscle differentiation medium (Cat# C‐23061, PromoCell, USA) provided by VWR International PBI S.r.l. in the presence or not of NaB 3 mM (Cat# 303410 Life Technologies), MK1903 (Cat# 4622, Tocris UK), or rosiglitazone (Cat# 5325, Tocris UK).

Techniques: Expressing, Control

A Schematic representation of miRNAs targeting the 3′‐UTR region of both murine and human CB1 gene. B Heatmap representation of the expression of selected miRNAs in the indicated biological replicates. Red—up‐regulated; green—down‐regulated. C–J Bar chart with individual points showing the expression of selected miRNAs in control and Gpr109A‐silenced C2C12 myoblasts exposed to LPS (1 μg/ml) in the presence or absence of either NaB (3 mM), MK1903 (1 μM), or rosiglitazone (1 μM). NaB was also tested in the presence or absence of either rosiglitazone (1 μM) or T007 (1 μM). Data Information: Each bar is the mean ± S.E.M. from 3 independent biological replicates. ± P ≤ 0.05 vs. veh group; ** P ≤ 0.03 vs. LPS group; # P ≤ 0.05 vs. the other experimental groups calculated using ANOVA.

Journal: EMBO Molecular Medicine

Article Title: Targeting gut dysbiosis against inflammation and impaired autophagy in Duchenne muscular dystrophy

doi: 10.15252/emmm.202216225

Figure Lengend Snippet: A Schematic representation of miRNAs targeting the 3′‐UTR region of both murine and human CB1 gene. B Heatmap representation of the expression of selected miRNAs in the indicated biological replicates. Red—up‐regulated; green—down‐regulated. C–J Bar chart with individual points showing the expression of selected miRNAs in control and Gpr109A‐silenced C2C12 myoblasts exposed to LPS (1 μg/ml) in the presence or absence of either NaB (3 mM), MK1903 (1 μM), or rosiglitazone (1 μM). NaB was also tested in the presence or absence of either rosiglitazone (1 μM) or T007 (1 μM). Data Information: Each bar is the mean ± S.E.M. from 3 independent biological replicates. ± P ≤ 0.05 vs. veh group; ** P ≤ 0.03 vs. LPS group; # P ≤ 0.05 vs. the other experimental groups calculated using ANOVA.

Article Snippet: Primary myoblasts were differentiated in myotubes using a commercially available skeletal muscle differentiation medium (Cat# C‐23061, PromoCell, USA) provided by VWR International PBI S.r.l. in the presence or not of NaB 3 mM (Cat# 303410 Life Technologies), MK1903 (Cat# 4622, Tocris UK), or rosiglitazone (Cat# 5325, Tocris UK).

Techniques: Expressing, Control

Main physico-chemical descriptors of the investigated drugs molecular properties.

Journal: Journal of Genetic Engineering & Biotechnology

Article Title: In silico and cheminformatics prediction with experimental validation of an adipogenesis cocktail, sorafenib with rosiglitazone for HCC dedifferentiation

doi: 10.1016/j.jgeb.2024.100429

Figure Lengend Snippet: Main physico-chemical descriptors of the investigated drugs molecular properties.

Article Snippet: Percentage distribution of the macromolecule targets of the small drug Rosiglitazone obtained via the Swiss institute of Bioinformatics (SIB) 2022 powered by ChemAxon SwissTargetPrediction.

Techniques:

Predicted biological activity of the  rosiglitazone  using the 2023 Molinspiration Cheminformatics bioactivity score v2022.08.

Journal: Journal of Genetic Engineering & Biotechnology

Article Title: In silico and cheminformatics prediction with experimental validation of an adipogenesis cocktail, sorafenib with rosiglitazone for HCC dedifferentiation

doi: 10.1016/j.jgeb.2024.100429

Figure Lengend Snippet: Predicted biological activity of the rosiglitazone using the 2023 Molinspiration Cheminformatics bioactivity score v2022.08.

Article Snippet: Percentage distribution of the macromolecule targets of the small drug Rosiglitazone obtained via the Swiss institute of Bioinformatics (SIB) 2022 powered by ChemAxon SwissTargetPrediction.

Techniques: Activity Assay

 Rosiglitazone  observations gene activities from ChEMBL library based on ChEMBL 20 in eukaryotes and SEA Search server predictions for targets.

Journal: Journal of Genetic Engineering & Biotechnology

Article Title: In silico and cheminformatics prediction with experimental validation of an adipogenesis cocktail, sorafenib with rosiglitazone for HCC dedifferentiation

doi: 10.1016/j.jgeb.2024.100429

Figure Lengend Snippet: Rosiglitazone observations gene activities from ChEMBL library based on ChEMBL 20 in eukaryotes and SEA Search server predictions for targets.

Article Snippet: Percentage distribution of the macromolecule targets of the small drug Rosiglitazone obtained via the Swiss institute of Bioinformatics (SIB) 2022 powered by ChemAxon SwissTargetPrediction.

Techniques: Membrane

3A. Percentage distribution of the macromolecule targets of the small drug Rosiglitazone obtained via the Swiss institute of Bioinformatics (SIB) 2022 powered by ChemAxon SwissTargetPrediction. Accessed Jan. 29th, 2023.

Journal: Journal of Genetic Engineering & Biotechnology

Article Title: In silico and cheminformatics prediction with experimental validation of an adipogenesis cocktail, sorafenib with rosiglitazone for HCC dedifferentiation

doi: 10.1016/j.jgeb.2024.100429

Figure Lengend Snippet: 3A. Percentage distribution of the macromolecule targets of the small drug Rosiglitazone obtained via the Swiss institute of Bioinformatics (SIB) 2022 powered by ChemAxon SwissTargetPrediction. Accessed Jan. 29th, 2023.

Article Snippet: Percentage distribution of the macromolecule targets of the small drug Rosiglitazone obtained via the Swiss institute of Bioinformatics (SIB) 2022 powered by ChemAxon SwissTargetPrediction.

Techniques:

HCC cell lines either Hep3B or HepG2 photographs examined microscopically using an inverted microscope for signs of morphological changes into adipocytes. Cells were stained with Oil Red O working solution. Magnification power x400. Control (Mock) group; HCC cell lines either HepG2 or Hep3B treated with free media, Group 2A: HCC cell lines, either HepG2 or Hep3B treated with 6 µM Sorafenib, 2 µM Rosiglitazone, and 0.5 µM IBMX, 0.86 µM Insulin and 1 µM Dexamethasone, Group 2B: HCC cell lines either HepG2 or Hep3B treated with 6 µM Sorafenib, 4 µM Rosiglitazone, and 0.5 µM IBMX, 0.86 µM Insulin and 1 µM Dexamethasone, Group 3A: HCC cell lines either HepG2 or Hep3B treated with 2 µM Rosiglitazone, and 0.5 µM IBMX, 0.86 µM Insulin and 1 µM Dexamethasone, and Group 3B: HCC cell lines either HepG2 or Hep3B treated with 4 µM Rosiglitazone, and 0.5 µM IBMX, 0.86 µM Insulin and 1 µM Dexamethasone. Magnification power is 400x. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.). (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

Journal: Journal of Genetic Engineering & Biotechnology

Article Title: In silico and cheminformatics prediction with experimental validation of an adipogenesis cocktail, sorafenib with rosiglitazone for HCC dedifferentiation

doi: 10.1016/j.jgeb.2024.100429

Figure Lengend Snippet: HCC cell lines either Hep3B or HepG2 photographs examined microscopically using an inverted microscope for signs of morphological changes into adipocytes. Cells were stained with Oil Red O working solution. Magnification power x400. Control (Mock) group; HCC cell lines either HepG2 or Hep3B treated with free media, Group 2A: HCC cell lines, either HepG2 or Hep3B treated with 6 µM Sorafenib, 2 µM Rosiglitazone, and 0.5 µM IBMX, 0.86 µM Insulin and 1 µM Dexamethasone, Group 2B: HCC cell lines either HepG2 or Hep3B treated with 6 µM Sorafenib, 4 µM Rosiglitazone, and 0.5 µM IBMX, 0.86 µM Insulin and 1 µM Dexamethasone, Group 3A: HCC cell lines either HepG2 or Hep3B treated with 2 µM Rosiglitazone, and 0.5 µM IBMX, 0.86 µM Insulin and 1 µM Dexamethasone, and Group 3B: HCC cell lines either HepG2 or Hep3B treated with 4 µM Rosiglitazone, and 0.5 µM IBMX, 0.86 µM Insulin and 1 µM Dexamethasone. Magnification power is 400x. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.). (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: Percentage distribution of the macromolecule targets of the small drug Rosiglitazone obtained via the Swiss institute of Bioinformatics (SIB) 2022 powered by ChemAxon SwissTargetPrediction.

Techniques: Inverted Microscopy, Staining, Control

Alteration of adipogenesis markers in HepG2-treated cells appearing as ADIPOR1 and E-cadherin. The control mock group 1 (Con), Rosiglitazone group (R1): cells treated with rosiglitazone conc. 41 μM, Group 4B: HCC cell line treated with 6 µM Sorafenib, 4 µM Rosiglitazone, 0.5 µM IBMX, 0.86 µM Insulin, and 1 µM Dexamethasone, Sorafenib group (Sora1): cells treated with sorafenib IC 50 conc. 6 μM to evaluate the impact of sorafenib's IC 50 value on its own, Group 5B: HCC cell line treated with 4 µM Rosiglitazone, and 0.5 µM IBMX, 0.86 µM Insulin and 1 µM Dexamethasone. [KDa: kilo Dalton.] Lysates were immunoblotted with an anti-ADIPOR1 antibody and anti-E-cadherin antibody. Representative immunoblot of ADIPOR1 protein, Adipo-R1 (49 kDa) and E-cad (125 kDa). Actin served as loading control.

Journal: Journal of Genetic Engineering & Biotechnology

Article Title: In silico and cheminformatics prediction with experimental validation of an adipogenesis cocktail, sorafenib with rosiglitazone for HCC dedifferentiation

doi: 10.1016/j.jgeb.2024.100429

Figure Lengend Snippet: Alteration of adipogenesis markers in HepG2-treated cells appearing as ADIPOR1 and E-cadherin. The control mock group 1 (Con), Rosiglitazone group (R1): cells treated with rosiglitazone conc. 41 μM, Group 4B: HCC cell line treated with 6 µM Sorafenib, 4 µM Rosiglitazone, 0.5 µM IBMX, 0.86 µM Insulin, and 1 µM Dexamethasone, Sorafenib group (Sora1): cells treated with sorafenib IC 50 conc. 6 μM to evaluate the impact of sorafenib's IC 50 value on its own, Group 5B: HCC cell line treated with 4 µM Rosiglitazone, and 0.5 µM IBMX, 0.86 µM Insulin and 1 µM Dexamethasone. [KDa: kilo Dalton.] Lysates were immunoblotted with an anti-ADIPOR1 antibody and anti-E-cadherin antibody. Representative immunoblot of ADIPOR1 protein, Adipo-R1 (49 kDa) and E-cad (125 kDa). Actin served as loading control.

Article Snippet: Percentage distribution of the macromolecule targets of the small drug Rosiglitazone obtained via the Swiss institute of Bioinformatics (SIB) 2022 powered by ChemAxon SwissTargetPrediction.

Techniques: Control, Western Blot

Cisplatin increases intracellular reactive oxygen species (ROS) levels. Cytosolic ROS ( A ) and mitochondrial superoxide ( B ) levels in PEA1 and PEA2 cells treated with cisplatin at indicated concentrations for 24 h were quantified by flow cytometry using H 2 DCFDA dye and MitoSOX, respectively. Data are represented as mean fluorescence intensity and expressed as mean ± S.E.M. from three independent experiments. Significance was assessed by two-tailed Student’s t -test (* p -value < 0.05, ns p -value > 0.05). Representative histograms of H 2 DCFDA and MitoSOX expression are shown in the overlay.

Journal: Antioxidants

Article Title: Decreased Levels of GSH Are Associated with Platinum Resistance in High-Grade Serous Ovarian Cancer

doi: 10.3390/antiox11081544

Figure Lengend Snippet: Cisplatin increases intracellular reactive oxygen species (ROS) levels. Cytosolic ROS ( A ) and mitochondrial superoxide ( B ) levels in PEA1 and PEA2 cells treated with cisplatin at indicated concentrations for 24 h were quantified by flow cytometry using H 2 DCFDA dye and MitoSOX, respectively. Data are represented as mean fluorescence intensity and expressed as mean ± S.E.M. from three independent experiments. Significance was assessed by two-tailed Student’s t -test (* p -value < 0.05, ns p -value > 0.05). Representative histograms of H 2 DCFDA and MitoSOX expression are shown in the overlay.

Article Snippet: In glutathione colorimetric detection assay, PEA1 and PEA2 cells were treated with 20 μM and 40 μM of cisplatin, respectively, for 30 min. To evaluate intracellular ROS levels, as well as for real-time PCR assays, PEA1 and PEA2 cells were treated with 10–20 μM and 20–40 μM of cisplatin, corresponding to the IC50 of each cell line (20 and 40 μM, respectively) and the relative half, for 24 h. Cisplatin (NSC 119875) was purchased from Selleckchem (Cat.

Techniques: Flow Cytometry, Fluorescence, Two Tailed Test, Expressing

Fig. 2. Representative chromatogram of a standard mixture solution of Metformin hydrochloride,

Journal: Proceedings of the YSU B: Chemical and Biological Sciences

Article Title: DEVELOPMENT OF A RAPID AND EFFICIENT METHOD FOR QUANTITATIVE DETERMINATION OF N-NITROSODIMETHYLAMINE IMPURITY BY HIGH-PERFORMANCE LIQUID CHROMATOGRAPHY IN METFORMIN HYDROCHLORIDE, LOSARTAN POTASSIUM, VALSARTAN AND RANITIDINE MEDICINAL RAW MATERIALS AND ITS PRODUCTS

doi: 10.46991/pysu:b/2021.55.3.296

Figure Lengend Snippet: Fig. 2. Representative chromatogram of a standard mixture solution of Metformin hydrochloride,

Article Snippet: Standards and reagents: Metformin hydrochloride (99.9%), Losartan potassium (99.2%), Valsartan (100%), Ranitidine (99.7%) (EDQM), formic acid (Merck), acetonitrile (Merck); methanol (Merck); N-nitrosodimethylamine 200 μg/mL in methanol (Merck), water was taken from Milli-QR reference water purification system.

Techniques: