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Millipore 15d-pgj2
Pretreatments with <t>15d-PGJ2</t> and GW9662 altered the EMT-related changes in PM2.5-exposed HK-2 cells. HK-2 cells were treated with 15d-PGJ2 or GW9662 24 h before PM2.5 exposure. (A) Cell morphology observed under a microscope (magnification, 100 × ). (B) Cell migration was assayed using the Transwell migration assay. (C) PM2.5-induced changes in the mRNA levels of EMT-related markers were mitigated or exacerbated by 15d-PGJ2 and GW9662, respectively. Data are presented in terms of mean ± standard deviation values. * p < 0.05, compared with the control group; # p < 0.05, compared with the PM2.5-exposed group.
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Pretreatments with 15d-PGJ2 and GW9662 altered the EMT-related changes in PM2.5-exposed HK-2 cells. HK-2 cells were treated with 15d-PGJ2 or GW9662 24 h before PM2.5 exposure. (A) Cell morphology observed under a microscope (magnification, 100 × ). (B) Cell migration was assayed using the Transwell migration assay. (C) PM2.5-induced changes in the mRNA levels of EMT-related markers were mitigated or exacerbated by 15d-PGJ2 and GW9662, respectively. Data are presented in terms of mean ± standard deviation values. * p < 0.05, compared with the control group; # p < 0.05, compared with the PM2.5-exposed group.

Journal: Current Research in Toxicology

Article Title: PPARγ activation ameliorates PM2.5-induced renal tubular injury by inhibiting ferroptosis and epithelial–mesenchymal transition

doi: 10.1016/j.crtox.2024.100189

Figure Lengend Snippet: Pretreatments with 15d-PGJ2 and GW9662 altered the EMT-related changes in PM2.5-exposed HK-2 cells. HK-2 cells were treated with 15d-PGJ2 or GW9662 24 h before PM2.5 exposure. (A) Cell morphology observed under a microscope (magnification, 100 × ). (B) Cell migration was assayed using the Transwell migration assay. (C) PM2.5-induced changes in the mRNA levels of EMT-related markers were mitigated or exacerbated by 15d-PGJ2 and GW9662, respectively. Data are presented in terms of mean ± standard deviation values. * p < 0.05, compared with the control group; # p < 0.05, compared with the PM2.5-exposed group.

Article Snippet: The PPARγ agonist 15d-PGJ2 and the PPARγ antagonist GW9662 were purchased from Cayman Chemicals (Ann Arbor, MI, USA).

Techniques: Microscopy, Migration, Transwell Migration Assay, Standard Deviation, Control

Effects of 15d-PGJ2 and GW966 on the ferroptosis susceptibility of PM2.5-exposed HK-2 cells. HK-2 cells were treated with 15d-PGJ2 or GW9662 24 h before PM2.5 exposure. (A) Iron contents. (B) Reduced glutathione level. (C) MDA level. (D) The detection of lipid peroxidation in live cells.

Journal: Current Research in Toxicology

Article Title: PPARγ activation ameliorates PM2.5-induced renal tubular injury by inhibiting ferroptosis and epithelial–mesenchymal transition

doi: 10.1016/j.crtox.2024.100189

Figure Lengend Snippet: Effects of 15d-PGJ2 and GW966 on the ferroptosis susceptibility of PM2.5-exposed HK-2 cells. HK-2 cells were treated with 15d-PGJ2 or GW9662 24 h before PM2.5 exposure. (A) Iron contents. (B) Reduced glutathione level. (C) MDA level. (D) The detection of lipid peroxidation in live cells.

Article Snippet: The PPARγ agonist 15d-PGJ2 and the PPARγ antagonist GW9662 were purchased from Cayman Chemicals (Ann Arbor, MI, USA).

Techniques: