ppar-γ Search Results


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  • 95
    Millipore ppar γ
    Gene expression of klotho (A) and <t>PPAR-γ</t> (D) . Western blot analysis of klotho protein expression (B) . Immunohistochemistry staining for klotho and representative microphotographs (magnification, ×40) showing cortical sections of the kidney and the quantitative analyses (C,E) . The data are expressed as the mean ± standard error of the mean. Groups: CTL ( n = 5), NX ( n = 5), LOS ( n = 5), and PROP ( n = 5). ∗ P
    Ppar γ, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 105 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Santa Cruz Biotechnology peroxisome proliferator activated receptors ppar γ
    ( A ) Sterol regulatory element-binding proteins(SREBP)-1c; ( B ) peroxisome <t>proliferator-activated</t> receptors <t>(PPAR)-γ;</t> ( C ) PPAR-α; ( D ) glucose transporter (GLUT)-2; and ( E ) phosphoenolpyruvate carboxykinase (PEPCK) protein expression in hepatic tissue normalized to the signal for β-actin (expressed in arbitrary units, a.u.); ( F ) representative bands of the proteins. Values are means ± standard error. There was a significant difference ( p ≤ 0.05) compared with the a SC group; b HF group; and c HFr group.
    Peroxisome Proliferator Activated Receptors Ppar γ, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 85/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Cell Signaling Technology Inc ppar peroxisome proliferator activated receptors γ
    ( A ) Sterol regulatory element-binding proteins(SREBP)-1c; ( B ) peroxisome <t>proliferator-activated</t> receptors <t>(PPAR)-γ;</t> ( C ) PPAR-α; ( D ) glucose transporter (GLUT)-2; and ( E ) phosphoenolpyruvate carboxykinase (PEPCK) protein expression in hepatic tissue normalized to the signal for β-actin (expressed in arbitrary units, a.u.); ( F ) representative bands of the proteins. Values are means ± standard error. There was a significant difference ( p ≤ 0.05) compared with the a SC group; b HF group; and c HFr group.
    Ppar Peroxisome Proliferator Activated Receptors γ, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 92/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ppar peroxisome proliferator activated receptors γ/product/Cell Signaling Technology Inc
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    99
    Millipore ppar γ antagonist
    FIGURE 7. Effects of <t>PPAR-γ</t> antagonist on androstenediol-mediated alterations in plasma IL-6 (A) and PGJ2 (B) at 5 hours after sham operation or trauma-hemorrhage (T-H). Data are mean ± SEM (n = 6 animals/group). * P
    Ppar γ Antagonist, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    4Gene ppar γ
    FIGURE 7. Effects of <t>PPAR-γ</t> antagonist on androstenediol-mediated alterations in plasma IL-6 (A) and PGJ2 (B) at 5 hours after sham operation or trauma-hemorrhage (T-H). Data are mean ± SEM (n = 6 animals/group). * P
    Ppar γ, supplied by 4Gene, used in various techniques. Bioz Stars score: 92/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ppar γ/product/4Gene
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    91
    Cell Signaling Technology Inc ppar γ
    (A) Effects of S -allyl cysteine (SAC) administration on the gene expression and protein levels of Peroxisome proliferators-activated receptor <t>(PPAR)-γ</t> in the liver. Animals were treated as described in Fig. 1 . PPAR-γ mRNA expression was measured as described in Methods. Values are means ± SEM ( n = 5–6). # p
    Ppar γ, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 91/100, based on 221 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Santa Cruz Biotechnology ppar γ
    Effect of HC (100, 200 and 400 mg/kg) on STZ-induced changes in the levels of expression of <t>PPAR-</t> γ in liver, pancreas, and adipose tissues. The blots (a) are representative of PPAR- γ in liver, pancreas, and adipose tissues. The results in the histogram (b) are expressed as ratio of relative intensity of levels of protein expression PPAR- γ to β -Actin. All values are mean ± SEM of three separate sets of independent experiments. a P
    Ppar γ, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 539 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Abcam ppar γ
    RGZ treatment promotes <t>PPAR-γ</t> activation. Western blot analysis was employed to assess PPAR-γ expression and activation by evaluating the levels of total PPAR-γ and activated PPAR-γ (p-PPAR-γ). (A) A representative result obtained by western blot analysis. (B) Semi-quantitative analysis of cells studied in each group. The relative amount of PPAR-γ and p-PPAR-γ in each group of cells was normalized by β-actin and presented as the ratio of p-PPAR-γ to PPAR-γ. ### P
    Ppar γ, supplied by Abcam, used in various techniques. Bioz Stars score: 92/100, based on 312 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    ZenBio ppar γ
    RGZ treatment promotes <t>PPAR-γ</t> activation. Western blot analysis was employed to assess PPAR-γ expression and activation by evaluating the levels of total PPAR-γ and activated PPAR-γ (p-PPAR-γ). (A) A representative result obtained by western blot analysis. (B) Semi-quantitative analysis of cells studied in each group. The relative amount of PPAR-γ and p-PPAR-γ in each group of cells was normalized by β-actin and presented as the ratio of p-PPAR-γ to PPAR-γ. ### P
    Ppar γ, supplied by ZenBio, used in various techniques. Bioz Stars score: 92/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Addgene inc ppar γ
    Hcy induces inflammation in human chondrocytes. Cells were treated with Hcy (100 μM) for 24 h. (A-B) Representative Western blots and quantification data showing that Hcy treatment downregulated <t>PPAR-γ</t> expression. (C) NF-κB activity was tested using a NF-κB activity kit. (D-E) MMP-13 and IL-8 levels were tested by ELISA assay. (F, G) COX-2 levels were tested by Western blotting assay. (Data are presented as the mean ± SD of three different experiments. * p
    Ppar γ, supplied by Addgene inc, used in various techniques. Bioz Stars score: 92/100, based on 16 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ppar γ/product/Addgene inc
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    92
    Lifespan Biosciences ppar γ
    Hcy induces inflammation in human chondrocytes. Cells were treated with Hcy (100 μM) for 24 h. (A-B) Representative Western blots and quantification data showing that Hcy treatment downregulated <t>PPAR-γ</t> expression. (C) NF-κB activity was tested using a NF-κB activity kit. (D-E) MMP-13 and IL-8 levels were tested by ELISA assay. (F, G) COX-2 levels were tested by Western blotting assay. (Data are presented as the mean ± SD of three different experiments. * p
    Ppar γ, supplied by Lifespan Biosciences, used in various techniques. Bioz Stars score: 92/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ppar γ/product/Lifespan Biosciences
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    93
    Unigene ppar γ
    Hcy induces inflammation in human chondrocytes. Cells were treated with Hcy (100 μM) for 24 h. (A-B) Representative Western blots and quantification data showing that Hcy treatment downregulated <t>PPAR-γ</t> expression. (C) NF-κB activity was tested using a NF-κB activity kit. (D-E) MMP-13 and IL-8 levels were tested by ELISA assay. (F, G) COX-2 levels were tested by Western blotting assay. (Data are presented as the mean ± SD of three different experiments. * p
    Ppar γ, supplied by Unigene, used in various techniques. Bioz Stars score: 93/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ppar γ/product/Unigene
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    91
    Proteintech ppar γ
    Up-regulation of β-catenin mediates 5-HT-induced <t>PPAR</t> γ reduction
    Ppar γ, supplied by Proteintech, used in various techniques. Bioz Stars score: 91/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Gene expression of klotho (A) and PPAR-γ (D) . Western blot analysis of klotho protein expression (B) . Immunohistochemistry staining for klotho and representative microphotographs (magnification, ×40) showing cortical sections of the kidney and the quantitative analyses (C,E) . The data are expressed as the mean ± standard error of the mean. Groups: CTL ( n = 5), NX ( n = 5), LOS ( n = 5), and PROP ( n = 5). ∗ P

    Journal: Frontiers in Physiology

    Article Title: Klotho and PPAR Gamma Activation Mediate the Renoprotective Effect of Losartan in the 5/6 Nephrectomy Model

    doi: 10.3389/fphys.2018.01033

    Figure Lengend Snippet: Gene expression of klotho (A) and PPAR-γ (D) . Western blot analysis of klotho protein expression (B) . Immunohistochemistry staining for klotho and representative microphotographs (magnification, ×40) showing cortical sections of the kidney and the quantitative analyses (C,E) . The data are expressed as the mean ± standard error of the mean. Groups: CTL ( n = 5), NX ( n = 5), LOS ( n = 5), and PROP ( n = 5). ∗ P

    Article Snippet: At semi-confluence, the cells were incubated with the respective drug, angiotensin II (10-12 , 10-10 , 10-8 , and 10-6 mol/L), losartan (10-8 mol/L), pioglitazone, an agonist of PPAR-γ (10-7 , 10-6 , and 10-5 mol/L), and/or BADGE, an antagonist of PPAR-γ (10-3 mol/L), for 24 h. All of the reagents were obtained from Sigma-Aldrich.

    Techniques: Expressing, Western Blot, Immunohistochemistry, Staining, CTL Assay

    Gene expression and PPAR-γ activation. Gene expression of klotho and PPAR-γ in MDCK cells (A–E) . PPAR-γ activity as assessed by an ELISA of MDCK cells (F) . The data are expressed as the mean ± standard error of the mean. ∗ P

    Journal: Frontiers in Physiology

    Article Title: Klotho and PPAR Gamma Activation Mediate the Renoprotective Effect of Losartan in the 5/6 Nephrectomy Model

    doi: 10.3389/fphys.2018.01033

    Figure Lengend Snippet: Gene expression and PPAR-γ activation. Gene expression of klotho and PPAR-γ in MDCK cells (A–E) . PPAR-γ activity as assessed by an ELISA of MDCK cells (F) . The data are expressed as the mean ± standard error of the mean. ∗ P

    Article Snippet: At semi-confluence, the cells were incubated with the respective drug, angiotensin II (10-12 , 10-10 , 10-8 , and 10-6 mol/L), losartan (10-8 mol/L), pioglitazone, an agonist of PPAR-γ (10-7 , 10-6 , and 10-5 mol/L), and/or BADGE, an antagonist of PPAR-γ (10-3 mol/L), for 24 h. All of the reagents were obtained from Sigma-Aldrich.

    Techniques: Expressing, Activation Assay, Activity Assay, Enzyme-linked Immunosorbent Assay

    PPAR- γ ligands decrease wound closure in MCF-10A cells. Ciglitazone (a) and 15d-PGJ2 (b) were added to cells, and wound-induced closure measured as detailed under Section 2 . Data shown are the 12-hour time point + SD ( n = 3) ** P

    Journal: Journal of Oncology

    Article Title: Peroxisome Proliferator-Activated Receptor-γ Ligands Alter Breast Cancer Cell Motility through Modulation of the Plasminogen Activator System

    doi: 10.1155/2011/594258

    Figure Lengend Snippet: PPAR- γ ligands decrease wound closure in MCF-10A cells. Ciglitazone (a) and 15d-PGJ2 (b) were added to cells, and wound-induced closure measured as detailed under Section 2 . Data shown are the 12-hour time point + SD ( n = 3) ** P

    Article Snippet: Modified-Boyden Chamber Assay Following serum starvation, cells were treated with PPAR-γ ligands ranging to 10 μ M of ciglitazone, ArA (ArA-sodium salt, Sigma, St. Louis, Mo, USA), or DhA (DhA-sodium salt, Sigma, St. Louis, Mo.

    Techniques:

    Modulation of PPAR-γ activity on lipid-induced macrophages M1/M2 polarization shifting. RAW264.7 macrophages were pre-incubated with either GW1929 (20 μmol/L) or GW9662 (60 μmol/L) for 3 h, followed by combined treatment with either PA (0.5 mmol/L) or DHA (50 μmol/L) for 6 h. Total RNA was extracted from treated RAW264.7 macrophages. ( A ) PPAR-γ agonist and antagonist affected PPAR-γ mRNA expression. ( B ) PPAR-γ agonist GW1929 flavored macrophages towards M2 phenotype shifting in PA-treated group. ( C ) PPAR-γ antagonist GW9662 enhanced M1 phenotype in PA-treated cells. All values are expressed as mean ± SEM, * P

    Journal: Scientific Reports

    Article Title: Effect of modulation of PPAR-γ activity on Kupffer cells M1/M2 polarization in the development of non-alcoholic fatty liver disease

    doi: 10.1038/srep44612

    Figure Lengend Snippet: Modulation of PPAR-γ activity on lipid-induced macrophages M1/M2 polarization shifting. RAW264.7 macrophages were pre-incubated with either GW1929 (20 μmol/L) or GW9662 (60 μmol/L) for 3 h, followed by combined treatment with either PA (0.5 mmol/L) or DHA (50 μmol/L) for 6 h. Total RNA was extracted from treated RAW264.7 macrophages. ( A ) PPAR-γ agonist and antagonist affected PPAR-γ mRNA expression. ( B ) PPAR-γ agonist GW1929 flavored macrophages towards M2 phenotype shifting in PA-treated group. ( C ) PPAR-γ antagonist GW9662 enhanced M1 phenotype in PA-treated cells. All values are expressed as mean ± SEM, * P

    Article Snippet: For PPAR-γ agonist or antagonist intervention, RAW264.7 macrophages were pre-incubated with either GW1929 (an agonist of PPAR-γ, 20 μmol/L, Sigma Aldrich) or GW9662 (an antagonist of PPAR-γ, 60 μmol/L, Sigma Aldrich) for 3 h, followed by combined treatment of different fatty acids with PPAR-γ agonist or antagonist as above.

    Techniques: Activity Assay, Incubation, Expressing

    Effect of PPAR-γ agonist on HF diet-induced Kupffer cells polarization and hepatic steatosis. Wild-type C57BL/6 mice were fed either NC diet or HF diet for 16 weeks. Rosiglitazone (30 mg/kg/d) by oral gavage once daily for 28 consecutive days began after 12 weeks of HF-diet feeding, PBS oral gavage served as control (n = 5/subgroup). Kupffer cells were isolated from NC diet, HF-diet alone or combined with rosiglitazone treatment mice. (A) M1/M2 gene markers expression on Kupffer cells, ( B ) M1/M2 phenotype Kupffer cells determined by Immunohistochemical staining (200× magnification), ( C ) Hepatic steatosis, ( D ) Body weight of mice, ( E ) Hepatic pro-inflammatory cytokines expression. Values are mean ± SEM, * P

    Journal: Scientific Reports

    Article Title: Effect of modulation of PPAR-γ activity on Kupffer cells M1/M2 polarization in the development of non-alcoholic fatty liver disease

    doi: 10.1038/srep44612

    Figure Lengend Snippet: Effect of PPAR-γ agonist on HF diet-induced Kupffer cells polarization and hepatic steatosis. Wild-type C57BL/6 mice were fed either NC diet or HF diet for 16 weeks. Rosiglitazone (30 mg/kg/d) by oral gavage once daily for 28 consecutive days began after 12 weeks of HF-diet feeding, PBS oral gavage served as control (n = 5/subgroup). Kupffer cells were isolated from NC diet, HF-diet alone or combined with rosiglitazone treatment mice. (A) M1/M2 gene markers expression on Kupffer cells, ( B ) M1/M2 phenotype Kupffer cells determined by Immunohistochemical staining (200× magnification), ( C ) Hepatic steatosis, ( D ) Body weight of mice, ( E ) Hepatic pro-inflammatory cytokines expression. Values are mean ± SEM, * P

    Article Snippet: For PPAR-γ agonist or antagonist intervention, RAW264.7 macrophages were pre-incubated with either GW1929 (an agonist of PPAR-γ, 20 μmol/L, Sigma Aldrich) or GW9662 (an antagonist of PPAR-γ, 60 μmol/L, Sigma Aldrich) for 3 h, followed by combined treatment of different fatty acids with PPAR-γ agonist or antagonist as above.

    Techniques: Mouse Assay, Isolation, Expressing, Immunohistochemistry, Staining

    PPAR γ activators inhibit IFN- γ -induced CXC chemokine mRNA expression in human ECs. A , Representative Northern blot analysis of ECs treated for 12 h with IFN- γ (100 U/ml) and PPAR γ activators (10 μ M 15d-PGJ 2 , 10 μ M troglitazone (trogl), 10 μ M BRL49653 (BRL); left panel ) or with PPAR α activators (30 μ M DHA, 30 μ M EPA, 250 μ M WY14643 (WY); right panel ). Ethanol (ETOH) as a solvent for PPAR activators served as control. B , Densitometry analysis of three independent Northern blot experiments described in A . Results of chemokine expression were normalized to GAPDH and are expressed as percent of IFN- γ -stimulated cells (% control). Bars represent mean ± SEM. *, p

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: Peroxisome Proliferator-Activated Receptor-γ Activators Inhibit IFN-γ-Induced Expression of the T Cell-Active CXC Chemokines IP-10, Mig, and I-TAC in Human Endothelial Cells

    doi:

    Figure Lengend Snippet: PPAR γ activators inhibit IFN- γ -induced CXC chemokine mRNA expression in human ECs. A , Representative Northern blot analysis of ECs treated for 12 h with IFN- γ (100 U/ml) and PPAR γ activators (10 μ M 15d-PGJ 2 , 10 μ M troglitazone (trogl), 10 μ M BRL49653 (BRL); left panel ) or with PPAR α activators (30 μ M DHA, 30 μ M EPA, 250 μ M WY14643 (WY); right panel ). Ethanol (ETOH) as a solvent for PPAR activators served as control. B , Densitometry analysis of three independent Northern blot experiments described in A . Results of chemokine expression were normalized to GAPDH and are expressed as percent of IFN- γ -stimulated cells (% control). Bars represent mean ± SEM. *, p

    Article Snippet: Human ECs were treated in standard culture media as above for 12 h with IFN- γ (100 U/ml) in the absence or presence of different PPAR γ activators (10 μ M 15d-PGJ2 (Calbiochem, La Jolla, CA), 10 μ M troglitazone (gift from Parke-Davis, Morris Plains, NJ), 10 μ M BRL49653 (rosiglitazone; gift from SmithKline Beecham, Philadelphia, PA)) or PPAR α activators (30 μ M docosahexaenoic acid (DHA), 30 μ M eicosapentaenoic acid (EPA) (both from Sigma, St. Louis, MO), and 250 μ M WY14643 (Biomol, Plymouth Meeting, PA)).

    Techniques: Expressing, Northern Blot

    PPAR γ activators inhibit IFN- γ -induced IP-10 promoter activity. A , Schematic of IP-10 promoter constructs used in transfection experiments. B , ECV304 cells were cotransfected with the two different IP-10 constructs shown in A and with a β -galactosidase expression construct (pCMV/ β -GAL). Transfected cells were stimulated with agents indicated for 16 h, and assays were performed for luciferase and β -galactosidase activity. Results for each construct were normalized to β -galactosidase activity and expressed as fold induction compared with unstimulated cells. Bars represent mean ± SEM ( n = 3), *, p

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: Peroxisome Proliferator-Activated Receptor-γ Activators Inhibit IFN-γ-Induced Expression of the T Cell-Active CXC Chemokines IP-10, Mig, and I-TAC in Human Endothelial Cells

    doi:

    Figure Lengend Snippet: PPAR γ activators inhibit IFN- γ -induced IP-10 promoter activity. A , Schematic of IP-10 promoter constructs used in transfection experiments. B , ECV304 cells were cotransfected with the two different IP-10 constructs shown in A and with a β -galactosidase expression construct (pCMV/ β -GAL). Transfected cells were stimulated with agents indicated for 16 h, and assays were performed for luciferase and β -galactosidase activity. Results for each construct were normalized to β -galactosidase activity and expressed as fold induction compared with unstimulated cells. Bars represent mean ± SEM ( n = 3), *, p

    Article Snippet: Human ECs were treated in standard culture media as above for 12 h with IFN- γ (100 U/ml) in the absence or presence of different PPAR γ activators (10 μ M 15d-PGJ2 (Calbiochem, La Jolla, CA), 10 μ M troglitazone (gift from Parke-Davis, Morris Plains, NJ), 10 μ M BRL49653 (rosiglitazone; gift from SmithKline Beecham, Philadelphia, PA)) or PPAR α activators (30 μ M docosahexaenoic acid (DHA), 30 μ M eicosapentaenoic acid (EPA) (both from Sigma, St. Louis, MO), and 250 μ M WY14643 (Biomol, Plymouth Meeting, PA)).

    Techniques: Activity Assay, Construct, Transfection, Expressing, Luciferase

    5-ASA binding assay for PPAR- γ . A competitive binding assay was performed with 40 nM [ 3 H]-rosiglitazone in the presence or absence of (A) PPAR-γ agonist GW1929 (0–800 nM, Sigma-Aldrich) used as positive control or (B) increasing concentrations of nonradioactive 5-ASA (0–100 mM). 5-ASA competed with rosiglitazone for binding to PPAR-γ. The specific binding obtained with [ 3 H]rosiglitazone alone was 100% of control. Results are expressed as the mean ± SEM in four different experiments.

    Journal: The Journal of Experimental Medicine

    Article Title: Intestinal antiinflammatory effect of 5-aminosalicylic acid is dependent on peroxisome proliferator-activated receptor-?

    doi: 10.1084/jem.20041948

    Figure Lengend Snippet: 5-ASA binding assay for PPAR- γ . A competitive binding assay was performed with 40 nM [ 3 H]-rosiglitazone in the presence or absence of (A) PPAR-γ agonist GW1929 (0–800 nM, Sigma-Aldrich) used as positive control or (B) increasing concentrations of nonradioactive 5-ASA (0–100 mM). 5-ASA competed with rosiglitazone for binding to PPAR-γ. The specific binding obtained with [ 3 H]rosiglitazone alone was 100% of control. Results are expressed as the mean ± SEM in four different experiments.

    Article Snippet: In brief, purified PPAR-γ–LBD (Invitrogen) was incubated at 4°C for 2–3 h in 100 μl of buffer A (50 mM Tris, pH 8.0, 100 mM KCl, 100 μg/ml OVA, 0.3% ([3-cholamidopropyl-dimethylammonio]-1-propanesulfonate), and 10 mM dithiothreitol) with 40 nM [3 H]rosiglitazone in the presence of increasing concentrations of unlabeled 5-ASA (0–100 mM) or the known PPAR-γ agonist GW1929 (0–800 nM, Sigma-Aldrich) used as positive control.

    Techniques: Binding Assay, Competitive Binding Assay, Positive Control

    PPAR-γ 2 expression of all depots and ages with and without ciglitazone.

    Journal: Annals of plastic surgery

    Article Title: Regional Anatomic and Age Effects on Cell Function of Human Adipose-Derived Stem Cells

    doi: 10.1097/SAP.0b013e3181723bbe

    Figure Lengend Snippet: PPAR-γ 2 expression of all depots and ages with and without ciglitazone.

    Article Snippet: Fifteen micrograms of PPAR-γ-2 protein were subjected to sodium dodecyl sulfate polyacrylamide gel electrophoresis fractionation, blotted onto nitrocellulose membrane, and probed with PPAR-γ-2 primary antibody (Cat MAB3872, Millipore, Billerica, MA).

    Techniques: Expressing

    The effect of PPAR γ knockdown in HepG2 cells on APOE, TOMM40 and APOC1 -mRNA levels. RNA was extracted from three HepG2 derived cell-lines: PPAR γ-shRNA (PPARγ KD), GFP-shRNA (GFP) and untransduced (U). The levels of (A) APOE -mRNA, (B) TOMM40 -mRNA, and (C) APOC1 -mRNA relative to the geometric mean of GAPDH and PPIA -mRNAs were assessed by real-time PCR and were analyzed by the 2 −ΔΔCt method. The different shRNA HepG2 cell-lines are indicated on the X-axis, and the fold change of mRNA (log2 transformed) is indicated on the Y-axis. The values presented here are means levels±SEM of 4 replicates. Tukey-Kramer HSD analysis was used to determine significant differences (*, p

    Journal: Biochimica et biophysica acta

    Article Title: The effects of PPARγ on the regulation of the TOMM40-APOE-C1 genes cluster

    doi: 10.1016/j.bbadis.2017.01.004

    Figure Lengend Snippet: The effect of PPAR γ knockdown in HepG2 cells on APOE, TOMM40 and APOC1 -mRNA levels. RNA was extracted from three HepG2 derived cell-lines: PPAR γ-shRNA (PPARγ KD), GFP-shRNA (GFP) and untransduced (U). The levels of (A) APOE -mRNA, (B) TOMM40 -mRNA, and (C) APOC1 -mRNA relative to the geometric mean of GAPDH and PPIA -mRNAs were assessed by real-time PCR and were analyzed by the 2 −ΔΔCt method. The different shRNA HepG2 cell-lines are indicated on the X-axis, and the fold change of mRNA (log2 transformed) is indicated on the Y-axis. The values presented here are means levels±SEM of 4 replicates. Tukey-Kramer HSD analysis was used to determine significant differences (*, p

    Article Snippet: We generated a HepG2 cell line with stable PPAR γ knockdown using a lentiviral shRNA clone, from the MISSION® TRC1 shRNA Library (Sigma® Life Science and The RNAi Consortium (TRC)).

    Techniques: Derivative Assay, shRNA, Real-time Polymerase Chain Reaction, Transformation Assay

    ( A ) Sterol regulatory element-binding proteins(SREBP)-1c; ( B ) peroxisome proliferator-activated receptors (PPAR)-γ; ( C ) PPAR-α; ( D ) glucose transporter (GLUT)-2; and ( E ) phosphoenolpyruvate carboxykinase (PEPCK) protein expression in hepatic tissue normalized to the signal for β-actin (expressed in arbitrary units, a.u.); ( F ) representative bands of the proteins. Values are means ± standard error. There was a significant difference ( p ≤ 0.05) compared with the a SC group; b HF group; and c HFr group.

    Journal: International Journal of Molecular Sciences

    Article Title: Hepatic Adverse Effects of Fructose Consumption Independent of Overweight/Obesity

    doi: 10.3390/ijms141121873

    Figure Lengend Snippet: ( A ) Sterol regulatory element-binding proteins(SREBP)-1c; ( B ) peroxisome proliferator-activated receptors (PPAR)-γ; ( C ) PPAR-α; ( D ) glucose transporter (GLUT)-2; and ( E ) phosphoenolpyruvate carboxykinase (PEPCK) protein expression in hepatic tissue normalized to the signal for β-actin (expressed in arbitrary units, a.u.); ( F ) representative bands of the proteins. Values are means ± standard error. There was a significant difference ( p ≤ 0.05) compared with the a SC group; b HF group; and c HFr group.

    Article Snippet: Immunoblotting The expression of the sterol regulatory element-binding proteins (SREBP)-1c (Santa Cruz Biotechnology, code sc-367, Santa Cruz, CA, USA), peroxisome proliferator-activated receptors (PPAR)-γ (Santa Cruz Biotecnology, code sc-7273), PPAR-α (Santa Cruz Biotechnology, code sc-9000), glucose transporter (GLUT)-2 (Millipore, cat #07-1402, Billiberica, MA, USA) and phosphoenolpyruvate carboxykinase (PEPCK) (Santa Cruz Biotechnology, code sc-32879), were detected by immunoblotting using rabbit polyclonal antibodies.

    Techniques: Binding Assay, Expressing

    ( A ) Sterol regulatory element-binding proteins (SREBP)-1c/peroxisome proliferator-activated receptors (PPAR)-α ratio; ( B ) PPAR-γ/PPAR-α ratio. Expressed in arbitrary units, a.u. SC, HF, HFr and HF/HFr. Values are means ± standard error. There was a significant difference ( p ≤ 0.05) compared with the a SC group; b HF group; and c HFr group.

    Journal: International Journal of Molecular Sciences

    Article Title: Hepatic Adverse Effects of Fructose Consumption Independent of Overweight/Obesity

    doi: 10.3390/ijms141121873

    Figure Lengend Snippet: ( A ) Sterol regulatory element-binding proteins (SREBP)-1c/peroxisome proliferator-activated receptors (PPAR)-α ratio; ( B ) PPAR-γ/PPAR-α ratio. Expressed in arbitrary units, a.u. SC, HF, HFr and HF/HFr. Values are means ± standard error. There was a significant difference ( p ≤ 0.05) compared with the a SC group; b HF group; and c HFr group.

    Article Snippet: Immunoblotting The expression of the sterol regulatory element-binding proteins (SREBP)-1c (Santa Cruz Biotechnology, code sc-367, Santa Cruz, CA, USA), peroxisome proliferator-activated receptors (PPAR)-γ (Santa Cruz Biotecnology, code sc-7273), PPAR-α (Santa Cruz Biotechnology, code sc-9000), glucose transporter (GLUT)-2 (Millipore, cat #07-1402, Billiberica, MA, USA) and phosphoenolpyruvate carboxykinase (PEPCK) (Santa Cruz Biotechnology, code sc-32879), were detected by immunoblotting using rabbit polyclonal antibodies.

    Techniques: Binding Assay

    FIGURE 7. Effects of PPAR-γ antagonist on androstenediol-mediated alterations in plasma IL-6 (A) and PGJ2 (B) at 5 hours after sham operation or trauma-hemorrhage (T-H). Data are mean ± SEM (n = 6 animals/group). * P

    Journal: Annals of Surgery

    Article Title: A Role of PPAR-? in Androstenediol-Mediated Salutary Effects on Cardiac Function Following Trauma-Hemorrhage

    doi: 10.1097/01.sla.0000217709.00863.82

    Figure Lengend Snippet: FIGURE 7. Effects of PPAR-γ antagonist on androstenediol-mediated alterations in plasma IL-6 (A) and PGJ2 (B) at 5 hours after sham operation or trauma-hemorrhage (T-H). Data are mean ± SEM (n = 6 animals/group). * P

    Article Snippet: To block PPAR-γ activity, a separate group of animals was treated with PPAR-γ antagonist, GW9662 (1 mg/kg BW, Sigma) intraperitoneally at the beginning of resuscitation with or without androstenediol administration.

    Techniques:

    FIGURE 6. Effects of PPAR-γ antagonist on androstenediol-mediated alterations in cardiac gene expression of IL-6 (A) and iNOS (B) at 5 hours after sham operation or trauma-hemorrhage (T-H). Data are mean ± SEM (n = 3–5 animals/group). * P

    Journal: Annals of Surgery

    Article Title: A Role of PPAR-? in Androstenediol-Mediated Salutary Effects on Cardiac Function Following Trauma-Hemorrhage

    doi: 10.1097/01.sla.0000217709.00863.82

    Figure Lengend Snippet: FIGURE 6. Effects of PPAR-γ antagonist on androstenediol-mediated alterations in cardiac gene expression of IL-6 (A) and iNOS (B) at 5 hours after sham operation or trauma-hemorrhage (T-H). Data are mean ± SEM (n = 3–5 animals/group). * P

    Article Snippet: To block PPAR-γ activity, a separate group of animals was treated with PPAR-γ antagonist, GW9662 (1 mg/kg BW, Sigma) intraperitoneally at the beginning of resuscitation with or without androstenediol administration.

    Techniques: Expressing

    FIGURE 5. Effects of PPAR-γ antagonist on androstenediol-mediated restoration of cardiac function at 5 hours after sham operation or trauma-hemorrhage (T-H). A, Cardiac output. B, +dp/dt max . C, −dp/dt max . Data are mean ± SEM (n = 6 animals/group). * P

    Journal: Annals of Surgery

    Article Title: A Role of PPAR-? in Androstenediol-Mediated Salutary Effects on Cardiac Function Following Trauma-Hemorrhage

    doi: 10.1097/01.sla.0000217709.00863.82

    Figure Lengend Snippet: FIGURE 5. Effects of PPAR-γ antagonist on androstenediol-mediated restoration of cardiac function at 5 hours after sham operation or trauma-hemorrhage (T-H). A, Cardiac output. B, +dp/dt max . C, −dp/dt max . Data are mean ± SEM (n = 6 animals/group). * P

    Article Snippet: To block PPAR-γ activity, a separate group of animals was treated with PPAR-γ antagonist, GW9662 (1 mg/kg BW, Sigma) intraperitoneally at the beginning of resuscitation with or without androstenediol administration.

    Techniques:

    (A) Effects of S -allyl cysteine (SAC) administration on the gene expression and protein levels of Peroxisome proliferators-activated receptor (PPAR)-γ in the liver. Animals were treated as described in Fig. 1 . PPAR-γ mRNA expression was measured as described in Methods. Values are means ± SEM ( n = 5–6). # p

    Journal: Journal of Clinical Biochemistry and Nutrition

    Article Title: S-Allyl cysteine improves nonalcoholic fatty liver disease in type 2 diabetes Otsuka Long-Evans Tokushima Fatty rats via regulation of hepatic lipogenesis and glucose metabolism

    doi: 10.3164/jcbn.13-1

    Figure Lengend Snippet: (A) Effects of S -allyl cysteine (SAC) administration on the gene expression and protein levels of Peroxisome proliferators-activated receptor (PPAR)-γ in the liver. Animals were treated as described in Fig. 1 . PPAR-γ mRNA expression was measured as described in Methods. Values are means ± SEM ( n = 5–6). # p

    Article Snippet: Nuclear and cytosol proteins (15–20 µg) were analyzed by immunoblotting for PPAR-α and PPAR-γ (Cell Signaling Technology, Inc.) as described above.

    Techniques: Expressing

    Effect of HC (100, 200 and 400 mg/kg) on STZ-induced changes in the levels of expression of PPAR- γ in liver, pancreas, and adipose tissues. The blots (a) are representative of PPAR- γ in liver, pancreas, and adipose tissues. The results in the histogram (b) are expressed as ratio of relative intensity of levels of protein expression PPAR- γ to β -Actin. All values are mean ± SEM of three separate sets of independent experiments. a P

    Journal: Advances in Pharmacological Sciences

    Article Title: Antihyperglycemic Activity of Houttuynia cordata Thunb. in Streptozotocin-Induced Diabetic Rats

    doi: 10.1155/2014/809438

    Figure Lengend Snippet: Effect of HC (100, 200 and 400 mg/kg) on STZ-induced changes in the levels of expression of PPAR- γ in liver, pancreas, and adipose tissues. The blots (a) are representative of PPAR- γ in liver, pancreas, and adipose tissues. The results in the histogram (b) are expressed as ratio of relative intensity of levels of protein expression PPAR- γ to β -Actin. All values are mean ± SEM of three separate sets of independent experiments. a P

    Article Snippet: Evaluation of Caspase-3, PPAR-γ , GLUT-2, and 4 by Western Blotting Caspase-3, PPAR-γ , GLUT-4, and 2 antibodies were purchased from Santa Cruz Biotechnology Inc (Santa Cruz, CA, USA).

    Techniques: Expressing

    RGZ treatment promotes PPAR-γ activation. Western blot analysis was employed to assess PPAR-γ expression and activation by evaluating the levels of total PPAR-γ and activated PPAR-γ (p-PPAR-γ). (A) A representative result obtained by western blot analysis. (B) Semi-quantitative analysis of cells studied in each group. The relative amount of PPAR-γ and p-PPAR-γ in each group of cells was normalized by β-actin and presented as the ratio of p-PPAR-γ to PPAR-γ. ### P

    Journal: Oncology Letters

    Article Title: Antitumor action of the peroxisome proliferator-activated receptor-γ agonist rosiglitazone in hepatocellular carcinoma

    doi: 10.3892/ol.2015.3554

    Figure Lengend Snippet: RGZ treatment promotes PPAR-γ activation. Western blot analysis was employed to assess PPAR-γ expression and activation by evaluating the levels of total PPAR-γ and activated PPAR-γ (p-PPAR-γ). (A) A representative result obtained by western blot analysis. (B) Semi-quantitative analysis of cells studied in each group. The relative amount of PPAR-γ and p-PPAR-γ in each group of cells was normalized by β-actin and presented as the ratio of p-PPAR-γ to PPAR-γ. ### P

    Article Snippet: The membranes were first blocked with 5% non-fat milk for 2 h at room temperature, prior to incubation with the following primary monoclonal anti-human antibodies: PPAR-γ, activated PPAR-γ (p-PPAR-γ; rabbit; 1:500; cat. no. ab195925; Abcam, Cambridge, UK), PPAR-γ (1:1,000; rabbit; cat. no. ab59256; Abcam) p85, p-p85, Akt, p-Akt, caspase 3 (rabbit; 1:500; cat. no. ab32351; Abcam), cleavage-caspase 3 (rabbit; 1:500; cat. no. ab2302; Abcam), Bax (rabbit; 1:1,000; cat. no. ab7977; Abcam), Bcl-2 (mouse; 1:500; cat. no. ab117115; Abcam), p-p85 (rabbit; 1:1,000; cat. no. 4228S; Cell Signaling Technology, Inc., Danvers, MA, USA), p85 (rabbit; 1:500; cat. no. 4292S; Cell Signaling Technology, Inc.), p-Akt (rabbit; 1:500; cat. no. 4060S; Cell Signaling Technology, Inc.), Akt (rabbit; 1:1,000; cat. no. 4685S; Cell Signaling Technology, Inc.) and β-actin (rabbit; 1:3,000; cat. no. ab6276; Abcam).

    Techniques: Activation Assay, Western Blot, Expressing

    Hcy induces inflammation in human chondrocytes. Cells were treated with Hcy (100 μM) for 24 h. (A-B) Representative Western blots and quantification data showing that Hcy treatment downregulated PPAR-γ expression. (C) NF-κB activity was tested using a NF-κB activity kit. (D-E) MMP-13 and IL-8 levels were tested by ELISA assay. (F, G) COX-2 levels were tested by Western blotting assay. (Data are presented as the mean ± SD of three different experiments. * p

    Journal: Redox Biology

    Article Title: Homocysteine causes dysfunction of chondrocytes and oxidative stress through repression of SIRT1/AMPK pathway: A possible link between hyperhomocysteinemia and osteoarthritis

    doi: 10.1016/j.redox.2018.01.010

    Figure Lengend Snippet: Hcy induces inflammation in human chondrocytes. Cells were treated with Hcy (100 μM) for 24 h. (A-B) Representative Western blots and quantification data showing that Hcy treatment downregulated PPAR-γ expression. (C) NF-κB activity was tested using a NF-κB activity kit. (D-E) MMP-13 and IL-8 levels were tested by ELISA assay. (F, G) COX-2 levels were tested by Western blotting assay. (Data are presented as the mean ± SD of three different experiments. * p

    Article Snippet: Human SIRT1, AMPK, PGC-1α and PPAR-γ were obtained from Addgene (Cambridge, MA, USA).

    Techniques: Western Blot, Expressing, Activity Assay, Enzyme-linked Immunosorbent Assay

    Hcy causes inflammation in human chondrocytes by modulation of SIRT1/AMPK/PGC-1/PPAR-γ/NF-κB pathway Cells were treated with Hcy (100 μM) for 24 h. In PDTC intervention group, PDTC was pretreated for 1 h before Hcy stimulation. (A) NF-κB activity was tested using a NF-κB activity kit. (B, C) MMP-13 and IL-8 levels were tested by ELISA assay. (D, F) COX-2 levels were tested by Western blotting assay. (Data are presented as the mean± SD of three different experiments. * p 0

    Journal: Redox Biology

    Article Title: Homocysteine causes dysfunction of chondrocytes and oxidative stress through repression of SIRT1/AMPK pathway: A possible link between hyperhomocysteinemia and osteoarthritis

    doi: 10.1016/j.redox.2018.01.010

    Figure Lengend Snippet: Hcy causes inflammation in human chondrocytes by modulation of SIRT1/AMPK/PGC-1/PPAR-γ/NF-κB pathway Cells were treated with Hcy (100 μM) for 24 h. In PDTC intervention group, PDTC was pretreated for 1 h before Hcy stimulation. (A) NF-κB activity was tested using a NF-κB activity kit. (B, C) MMP-13 and IL-8 levels were tested by ELISA assay. (D, F) COX-2 levels were tested by Western blotting assay. (Data are presented as the mean± SD of three different experiments. * p 0

    Article Snippet: Human SIRT1, AMPK, PGC-1α and PPAR-γ were obtained from Addgene (Cambridge, MA, USA).

    Techniques: Pyrolysis Gas Chromatography, Activity Assay, Enzyme-linked Immunosorbent Assay, Western Blot

    Up-regulation of β-catenin mediates 5-HT-induced PPAR γ reduction

    Journal: Oncotarget

    Article Title: 5-HT induces PPAR γ reduction and proliferation of pulmonary artery smooth muscle cells via modulating GSK-3β/β-catenin pathway

    doi: 10.18632/oncotarget.20582

    Figure Lengend Snippet: Up-regulation of β-catenin mediates 5-HT-induced PPAR γ reduction

    Article Snippet: Polyclonal or monoclonal antibodies against phosphor-Akt, total-Akt, phosphor-GSK-3β, total-GSK-3β, β-catenin (Cell Signaling Technology, Beverly, MA, USA, 1:1000 dilution), PPAR γ (Proteintech Group, Chicago, IL, USA, 1:500 dilution) as well as GAPDH (Sigma, 1:2000 dilution) were used according to the manufacturer's protocols.

    Techniques:

    5-HT suppresses PPAR γ expression in PASMCs

    Journal: Oncotarget

    Article Title: 5-HT induces PPAR γ reduction and proliferation of pulmonary artery smooth muscle cells via modulating GSK-3β/β-catenin pathway

    doi: 10.18632/oncotarget.20582

    Figure Lengend Snippet: 5-HT suppresses PPAR γ expression in PASMCs

    Article Snippet: Polyclonal or monoclonal antibodies against phosphor-Akt, total-Akt, phosphor-GSK-3β, total-GSK-3β, β-catenin (Cell Signaling Technology, Beverly, MA, USA, 1:1000 dilution), PPAR γ (Proteintech Group, Chicago, IL, USA, 1:500 dilution) as well as GAPDH (Sigma, 1:2000 dilution) were used according to the manufacturer's protocols.

    Techniques: Expressing

    5-HT inactivates GSK-3β, up-regulates β-catenin and reduces PPAR γ by PI3K/Akt pathway

    Journal: Oncotarget

    Article Title: 5-HT induces PPAR γ reduction and proliferation of pulmonary artery smooth muscle cells via modulating GSK-3β/β-catenin pathway

    doi: 10.18632/oncotarget.20582

    Figure Lengend Snippet: 5-HT inactivates GSK-3β, up-regulates β-catenin and reduces PPAR γ by PI3K/Akt pathway

    Article Snippet: Polyclonal or monoclonal antibodies against phosphor-Akt, total-Akt, phosphor-GSK-3β, total-GSK-3β, β-catenin (Cell Signaling Technology, Beverly, MA, USA, 1:1000 dilution), PPAR γ (Proteintech Group, Chicago, IL, USA, 1:500 dilution) as well as GAPDH (Sigma, 1:2000 dilution) were used according to the manufacturer's protocols.

    Techniques:

    GSK-3β insufficiency or inhibition of proteasome activity up-regulates β-catenin and reduces PPAR γ

    Journal: Oncotarget

    Article Title: 5-HT induces PPAR γ reduction and proliferation of pulmonary artery smooth muscle cells via modulating GSK-3β/β-catenin pathway

    doi: 10.18632/oncotarget.20582

    Figure Lengend Snippet: GSK-3β insufficiency or inhibition of proteasome activity up-regulates β-catenin and reduces PPAR γ

    Article Snippet: Polyclonal or monoclonal antibodies against phosphor-Akt, total-Akt, phosphor-GSK-3β, total-GSK-3β, β-catenin (Cell Signaling Technology, Beverly, MA, USA, 1:1000 dilution), PPAR γ (Proteintech Group, Chicago, IL, USA, 1:500 dilution) as well as GAPDH (Sigma, 1:2000 dilution) were used according to the manufacturer's protocols.

    Techniques: Inhibition, Activity Assay

    Up-regulation of β-catenin and subsequent PPAR γ reduction mediates 5-HT-stimulated PASMCs proliferation

    Journal: Oncotarget

    Article Title: 5-HT induces PPAR γ reduction and proliferation of pulmonary artery smooth muscle cells via modulating GSK-3β/β-catenin pathway

    doi: 10.18632/oncotarget.20582

    Figure Lengend Snippet: Up-regulation of β-catenin and subsequent PPAR γ reduction mediates 5-HT-stimulated PASMCs proliferation

    Article Snippet: Polyclonal or monoclonal antibodies against phosphor-Akt, total-Akt, phosphor-GSK-3β, total-GSK-3β, β-catenin (Cell Signaling Technology, Beverly, MA, USA, 1:1000 dilution), PPAR γ (Proteintech Group, Chicago, IL, USA, 1:500 dilution) as well as GAPDH (Sigma, 1:2000 dilution) were used according to the manufacturer's protocols.

    Techniques: