pparγ agonist pioglitazone pgz  (MedChemExpress)

Journal: PLOS One

Article Title: Investigation of the effect and mechanisms of moxa smoke in the treatment of Influenza A Virus (IAV) infection

doi: 10.1371/journal.pone.0337906

Figure Lengend Snippet: The measurement of p-STAT3, STAT3, and PPARγ through western blot analysis (n = 6). All data are expressed as means ± standard error of the mean (SEM). Statistical significance was determined in comparison to the model group, with thresholds set at * p < 0.05, ** p < 0.01, and *** p < 0.001.

Article Snippet: The PPARγ agonist Pioglitazone (PGZ; MCE, USA) was administered via oral gavage at a dosage of 60 mg/kg/day [ ], commencing 4 day prior to PR8 nasal instillation and continuing for a total of 9 days until the animals were euthanized.

Techniques: Western Blot, Comparison

Journal: Frontiers in Pharmacology

Article Title: Stromal vascular fraction inhibits renal fibrosis by regulating metabolism and inflammation in obstructive nephropathy

doi: 10.3389/fphar.2025.1559446

Figure Lengend Snippet: SVF promoted PPAR activation and inhibited EMT in TCMK-1 cells (A) Immunoblots and quantification of PPARα and PPARγ in UUO kidneys from control and SVF-treated mice (n = 3). (B) Immunoblots and (C) quantification of PPARα, PPARγ, FN, αSMA, and E-cad in TCMK-1 cells treated with or without SVF (n = 3). (D) qPCR analysis for Fn1 , Col1a2 , and Acta2 in TCMK-1 cells treated with or without SVF (n = 4). (E) Immunoblots and (F) quantification of PPARα, PPARγ, FN, Col I, αSMA, and E-cad in TCMK-1 cells treated with SVF or SVF and pioglitazone combined (n = 3). (G) qPCR analysis for Fn1 , Col1a2 , and Acta2 in TCMK-1 cells treated with SVF or SVF and pioglitazone combined (n = 4). (H) qPCR analysis for Fn1 , Col1a2 , Acta2 , and Cdh1 in TCMK-1 cells treated with SVF or SVF and T0070907 combined (n = 4). The results represent mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, NS no significant.

Article Snippet: The PPARγ agonist pioglitazone (S2590, Selleck) and antagonist T0070907 (S2871, Selleck) were used.

Techniques: Activation Assay, Western Blot, Control

Journal: Frontiers in Pharmacology

Article Title: Stromal vascular fraction inhibits renal fibrosis by regulating metabolism and inflammation in obstructive nephropathy

doi: 10.3389/fphar.2025.1559446

Figure Lengend Snippet: Pharmacological activation of PPAR alleviated UUO-induced renal fibrosis and inflammation (A) Immunoblots and quantification of PPARα and PPARγ in UUO kidneys from control and pioglitazone-treated mice (n = 3). (B) Representative Masson staining and quantification of UUO kidneys from control and pioglitazone-treated mice (n = 5), scale bar = 40 μm. Asterisks (*) indicate regions of interstitial collagen deposition (in blue) (C) Immunoblots and quantification of FN, Col I, αSMA, E-cad, and N-cad expression in UUO kidneys from control and pioglitazone-treated mice (n = 3). (D,E) qPCR analysis for Col1a2 , Il1b , and Tnf in UUO kidneys from control and pioglitazone-treated mice (n = 5). The results represent mean ± SEM. *p < 0.05, **p < 0.01.

Article Snippet: The PPARγ agonist pioglitazone (S2590, Selleck) and antagonist T0070907 (S2871, Selleck) were used.

Techniques: Activation Assay, Western Blot, Control, Staining, Expressing

Journal: Molecular Medicine Reports

Article Title: PDCD4 promotes inflammation/fibrosis by activating the PPAR‑γ/NF‑κB pathway in mouse atrial myocytes

doi: 10.3892/mmr.2024.13333

Figure Lengend Snippet: mRNA and protein expression levels of PDCD4 in HL-1 cells after PDCD4 overexpression and silencing. (A) Transcriptional and (B) translational analysis of PDCD4 after oePDCD4 transfection by RT-qPCR and western blotting. (C) Statistical analysis of western blotting. **P<0.01, ***P<0.001 vs. oeNC. (D) Transcriptional and (E) translational analysis of PDCD4 after siPDCD4 transfection by RT-qPCR and western blotting. (F) Statistical analysis of western blotting. **P<0.01, ***P<0.001 vs. siNC. n=3. PDCD4, programmed cell death factor 4; RT-qPCR, reverse transcription-quantitative PCR; oe, overexpression; NC, negative control; si, small interfering.

Article Snippet: The HL-1 cells in the overexpression group were further divided into four groups as follows: i) oeNC; ii) oePDCD4; iii) oePDCD4 + PPARγ agonist (Pio; 0, 1.25, 2.5, 5, 10, 20, 40 and 80 µM, cat. no. HY-14601; MedChemExpress); and iv) oePDCD4 + NF-κB inhibitor (CBL0137; 0, 0.125, 0.25, 0.5, 1, 2, 4 and 8 µM, cat. no. HY-18935A; MedChemExpress).

Techniques: Expressing, Over Expression, Transfection, Quantitative RT-PCR, Western Blot, Reverse Transcription, Real-time Polymerase Chain Reaction, Negative Control

Journal: Molecular Medicine Reports

Article Title: PDCD4 promotes inflammation/fibrosis by activating the PPAR‑γ/NF‑κB pathway in mouse atrial myocytes

doi: 10.3892/mmr.2024.13333

Figure Lengend Snippet: Levels of fibrosis-associated proteins and inflammatory-related cytokines in oePDCD4-HL-1 cells. (A) Western blotting indicated that the upregulated protein expression levels of collagen I, collagen III, fibronectin, α-SMA and MMP2 in oe-PDCD4-HL-1 cells were attenuated by Pio and CBL0137. (B) Statistical analysis of western blotting. (C) Enzyme-linked immunosorbent assays showed that the upregulated protein concentrations of IL-6, IL-17A, IFN-γ and TNF-α, and downregulated protein concentration of IL-4, in oe-PDCD4-HL-1 cells were reversed by Pio and CBL0137. ***P<0.001 vs. oeNC; ### P<0.001 vs. oe-PDCD4. n=3. oe, overexpression; PDCD4, programmed cell death factor 4; α-SMA, α-smooth muscle actin; MMP, matrix metalloproteinase; Pio, pioglitazone hydrochloride; NC, negative control.

Article Snippet: The HL-1 cells in the overexpression group were further divided into four groups as follows: i) oeNC; ii) oePDCD4; iii) oePDCD4 + PPARγ agonist (Pio; 0, 1.25, 2.5, 5, 10, 20, 40 and 80 µM, cat. no. HY-14601; MedChemExpress); and iv) oePDCD4 + NF-κB inhibitor (CBL0137; 0, 0.125, 0.25, 0.5, 1, 2, 4 and 8 µM, cat. no. HY-18935A; MedChemExpress).

Techniques: Western Blot, Expressing, Protein Concentration, Over Expression, Negative Control

Journal: Molecular Medicine Reports

Article Title: PDCD4 promotes inflammation/fibrosis by activating the PPAR‑γ/NF‑κB pathway in mouse atrial myocytes

doi: 10.3892/mmr.2024.13333

Figure Lengend Snippet: Expression of PPARγ and PDCD4 in oePDCD4-HL-1 cells. (A) Western blotting indicated that the downregulated protein expression levels of PPARγ and upregulated protein expression levels of PDCD4 in oe-PDCD4-HL-1 cells were attenuated by Pio and CBL0137. (B) Statistical analysis of western blotting. ***P<0.001 vs. oeNC; ### P<0.001 vs. oe-PDCD4. n=3. PPARγ, peroxisome proliferator-activated receptor γ; PDCD4, programmed cell death factor 4; oe, overexpression; Pio, pioglitazone hydrochloride; NC, negative control.

Article Snippet: The HL-1 cells in the overexpression group were further divided into four groups as follows: i) oeNC; ii) oePDCD4; iii) oePDCD4 + PPARγ agonist (Pio; 0, 1.25, 2.5, 5, 10, 20, 40 and 80 µM, cat. no. HY-14601; MedChemExpress); and iv) oePDCD4 + NF-κB inhibitor (CBL0137; 0, 0.125, 0.25, 0.5, 1, 2, 4 and 8 µM, cat. no. HY-18935A; MedChemExpress).

Techniques: Expressing, Western Blot, Over Expression, Negative Control

Journal: Molecular Medicine Reports

Article Title: PDCD4 promotes inflammation/fibrosis by activating the PPAR‑γ/NF‑κB pathway in mouse atrial myocytes

doi: 10.3892/mmr.2024.13333

Figure Lengend Snippet: Expression of NF-κB subunits in oePDCD4-HL-1. (A) Western blotting indicated that, compared with in the oeNC group, the Nu p-p65/p65 ratio and Nu p-p50/PCNA ratio were increased in the oePDCD4 group, and these findings were partially reversed by Pio and CBL0137. However, there was no significant change in Cy p-p65/p65 ratio and Cy p-p50/GAPDH ratio among the four groups. (B) Statistical analysis of western blotting. (C) Immunofluorescence analysis showed that the increased protein expression of p-p65 in oe-PDCD4-HL-1 cells was attenuated by Pio and CBL0137. (D) Statistical analysis of fluorescence intensity. ***P<0.001 vs. oeNC; ### P<0.001 vs. oe-PDCD4. n=3. Magnification, ×1,000. oe, overexpression; PDCD4, programmed cell death factor 4; NC, negative control; p-, phosphorylated; PCNA, proliferating cell nuclear antigen; Pio, pioglitazone hydrochloride; Nu, nuclear; Cy, cytoplasmic; NC, negative control.

Article Snippet: The HL-1 cells in the overexpression group were further divided into four groups as follows: i) oeNC; ii) oePDCD4; iii) oePDCD4 + PPARγ agonist (Pio; 0, 1.25, 2.5, 5, 10, 20, 40 and 80 µM, cat. no. HY-14601; MedChemExpress); and iv) oePDCD4 + NF-κB inhibitor (CBL0137; 0, 0.125, 0.25, 0.5, 1, 2, 4 and 8 µM, cat. no. HY-18935A; MedChemExpress).

Techniques: Expressing, Western Blot, Immunofluorescence, Fluorescence, Over Expression, Negative Control

Journal: International journal of molecular sciences

Article Title: Pioglitazone Modifies Kupffer Cell Function and Protects against Escherichia coli -Induced Bacteremia in Burned Mice.

doi: 10.3390/ijms232112746

Figure Lengend Snippet: Figure 3. Peroxisome proliferator-activated receptor gamma (PPARγ) antagonist, GW9662, abolishes the protective effects of pioglitazone in post-burn infection. (A) Survival of burned mice after intravenous infection with E. coli (5 × 108 CFU). Serum concentration of TNF at 1 h (B), IL-10 at 6 h (C), and ALT at 24 h (D) after infection. n = 15 per group; pooled data of two independent experiments. Data are represented as the mean ± SD.

Article Snippet: Five days after injury, mice were randomized to receive either the PPARγ agonist, pioglitazone (10 mg/kg; Santa Cruz, CA, USA) or vehicle control (10% v/v dimethyl sulfoxide in sterile saline) via intraperitoneal injection.

Techniques: Infection, Concentration Assay