pparg Search Results


95
Thermo Fisher gene exp pparg hs00234592 m1
BPZ disrupts fatty acids utilisation in human ovarian GCs. Schematic representation of fatty acids utilization and inhibitory action of Etomoxir ( A ). Oxygen consumption rate (OCR) changes post BPZ treatment in fatty acids dependency ( B ) and capacity ( C ) tests. BPZ-induced changes in fatty acids dependency, capacity and flexibility in primary GCs ( D , E , F ). Effects of BPZ on mRNA expression of fatty acids transporters, SLC27A1 ( G ) and CD36 ( H ) in HGrC1 cells. PPARA ( I ), PPARD ( J ) and <t>PPARG</t> ( K ) mRNA expression after BPZ treatment in primary GCs. Fatty acids uptake in primary GCs after 6 h BPZ treatment ( L ). Changes in viability post BPZ, fatty acids dependent pathway inhibitor, Etomoxir and co-treatment with both in HGrC1 cells ( M ). C, control (0.1% DMSO). Data are mean ± SD of three independent experiments. ** p ≤ 0.01; control vs. experimental group ( D – I ). Statistically significant are the mean values not sharing letters, p ≤ 0.05; pairwise comparison between each experimental group and the control ( J )
Gene Exp Pparg Hs00234592 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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92
OriGene myc pparγ protein
BPZ disrupts fatty acids utilisation in human ovarian GCs. Schematic representation of fatty acids utilization and inhibitory action of Etomoxir ( A ). Oxygen consumption rate (OCR) changes post BPZ treatment in fatty acids dependency ( B ) and capacity ( C ) tests. BPZ-induced changes in fatty acids dependency, capacity and flexibility in primary GCs ( D , E , F ). Effects of BPZ on mRNA expression of fatty acids transporters, SLC27A1 ( G ) and CD36 ( H ) in HGrC1 cells. PPARA ( I ), PPARD ( J ) and <t>PPARG</t> ( K ) mRNA expression after BPZ treatment in primary GCs. Fatty acids uptake in primary GCs after 6 h BPZ treatment ( L ). Changes in viability post BPZ, fatty acids dependent pathway inhibitor, Etomoxir and co-treatment with both in HGrC1 cells ( M ). C, control (0.1% DMSO). Data are mean ± SD of three independent experiments. ** p ≤ 0.01; control vs. experimental group ( D – I ). Statistically significant are the mean values not sharing letters, p ≤ 0.05; pairwise comparison between each experimental group and the control ( J )
Myc Pparγ Protein, supplied by OriGene, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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91
Biorbyt anti ppar γ
BPZ disrupts fatty acids utilisation in human ovarian GCs. Schematic representation of fatty acids utilization and inhibitory action of Etomoxir ( A ). Oxygen consumption rate (OCR) changes post BPZ treatment in fatty acids dependency ( B ) and capacity ( C ) tests. BPZ-induced changes in fatty acids dependency, capacity and flexibility in primary GCs ( D , E , F ). Effects of BPZ on mRNA expression of fatty acids transporters, SLC27A1 ( G ) and CD36 ( H ) in HGrC1 cells. PPARA ( I ), PPARD ( J ) and <t>PPARG</t> ( K ) mRNA expression after BPZ treatment in primary GCs. Fatty acids uptake in primary GCs after 6 h BPZ treatment ( L ). Changes in viability post BPZ, fatty acids dependent pathway inhibitor, Etomoxir and co-treatment with both in HGrC1 cells ( M ). C, control (0.1% DMSO). Data are mean ± SD of three independent experiments. ** p ≤ 0.01; control vs. experimental group ( D – I ). Statistically significant are the mean values not sharing letters, p ≤ 0.05; pairwise comparison between each experimental group and the control ( J )
Anti Ppar γ, supplied by Biorbyt, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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96
Proteintech anti pparγ
BPZ disrupts fatty acids utilisation in human ovarian GCs. Schematic representation of fatty acids utilization and inhibitory action of Etomoxir ( A ). Oxygen consumption rate (OCR) changes post BPZ treatment in fatty acids dependency ( B ) and capacity ( C ) tests. BPZ-induced changes in fatty acids dependency, capacity and flexibility in primary GCs ( D , E , F ). Effects of BPZ on mRNA expression of fatty acids transporters, SLC27A1 ( G ) and CD36 ( H ) in HGrC1 cells. PPARA ( I ), PPARD ( J ) and <t>PPARG</t> ( K ) mRNA expression after BPZ treatment in primary GCs. Fatty acids uptake in primary GCs after 6 h BPZ treatment ( L ). Changes in viability post BPZ, fatty acids dependent pathway inhibitor, Etomoxir and co-treatment with both in HGrC1 cells ( M ). C, control (0.1% DMSO). Data are mean ± SD of three independent experiments. ** p ≤ 0.01; control vs. experimental group ( D – I ). Statistically significant are the mean values not sharing letters, p ≤ 0.05; pairwise comparison between each experimental group and the control ( J )
Anti Pparγ, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
Proteintech pparg
Fig. 5 Kaempferol modulated estrogen metabolism pathways and differentially regulates <t>PPARG</t> expression in EC cells of different ER subtypes. A– <t>B</t> <t>HSD17B1</t> and HSD17B1-associated genes, such as ESRRA, PPARG, and ESR1, are involved in several estrogen metabolism pathways, such as steroid binding, 17- beta-hydroxysteroid dehydrogenase (NADP+) activity, steroid hormone biosynthesis, and regulation of hormone levels. C Kaempferol suppressed the expression of PPARG in ER-positive AN3 CA and promoted the expression of PPARG in ER-negative HEC-1-A. D–I Kaempferol suppressed the expression of PPARGC1A and ESRRA in both AN3 CA (D–F) and HEC-1-A cells (G–I), without modulating ESR1. Western blotting (D–E and G–H) and the IHC scores (F and I) confirmed the differential expression of PPARGC1A and ESRRA. Results are presented as means and SDs. Compared with the negative control, *, #P < 0.05, **, ##P < 0.01, ***, ###P < 0.001
Pparg, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pparg/PPARG+Antibody/pm36932403-186-59-67
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94
Proteintech anti pparg
Fig. 5 Kaempferol modulated estrogen metabolism pathways and differentially regulates <t>PPARG</t> expression in EC cells of different ER subtypes. A– <t>B</t> <t>HSD17B1</t> and HSD17B1-associated genes, such as ESRRA, PPARG, and ESR1, are involved in several estrogen metabolism pathways, such as steroid binding, 17- beta-hydroxysteroid dehydrogenase (NADP+) activity, steroid hormone biosynthesis, and regulation of hormone levels. C Kaempferol suppressed the expression of PPARG in ER-positive AN3 CA and promoted the expression of PPARG in ER-negative HEC-1-A. D–I Kaempferol suppressed the expression of PPARGC1A and ESRRA in both AN3 CA (D–F) and HEC-1-A cells (G–I), without modulating ESR1. Western blotting (D–E and G–H) and the IHC scores (F and I) confirmed the differential expression of PPARGC1A and ESRRA. Results are presented as means and SDs. Compared with the negative control, *, #P < 0.05, **, ##P < 0.01, ***, ###P < 0.001
Anti Pparg, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pparg/PPAR+gamma+Antibody/pmc06351131-301-65-66
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95
ABclonal Biotechnology anti hrd1 rb a11183 abclonal
Fig. 5 Kaempferol modulated estrogen metabolism pathways and differentially regulates <t>PPARG</t> expression in EC cells of different ER subtypes. A– <t>B</t> <t>HSD17B1</t> and HSD17B1-associated genes, such as ESRRA, PPARG, and ESR1, are involved in several estrogen metabolism pathways, such as steroid binding, 17- beta-hydroxysteroid dehydrogenase (NADP+) activity, steroid hormone biosynthesis, and regulation of hormone levels. C Kaempferol suppressed the expression of PPARG in ER-positive AN3 CA and promoted the expression of PPARG in ER-negative HEC-1-A. D–I Kaempferol suppressed the expression of PPARGC1A and ESRRA in both AN3 CA (D–F) and HEC-1-A cells (G–I), without modulating ESR1. Western blotting (D–E and G–H) and the IHC scores (F and I) confirmed the differential expression of PPARGC1A and ESRRA. Results are presented as means and SDs. Compared with the negative control, *, #P < 0.05, **, ##P < 0.01, ***, ###P < 0.001
Anti Hrd1 Rb A11183 Abclonal, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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94
ABclonal Biotechnology pparγ
ZQC regulates lipid metabolism via the <t>PPARγ</t> pathway in HG/PA-induced HepG2 cells. (A,B) Intracellular TG and T-CHO levels. (C,D) Relative expression of proteins <t>(e.g.,</t> <t>SREBP-1c,</t> ACC1). (E–H) WB quantification of representative lipogenic and PPARγ pathway proteins (FASN, PPARγ, CD36, FABP4) in control, HG/PA, HG/PA + 5% ZQC-S, and HG/PA + 7.5% ZQC-S groups. (I) Representative Oil Red O staining images of lipid droplets. (J) Quantification of lipid droplet content (ORO%) in each group. (K,L) Intracellular TG and T-CHO levels. (M) WB analysis of key proteins in control, HG/PA, HG/PA + 7.5% ZQC-S, and HG/PA + 7.5% ZQC-S + GW1929 groups. (N–S) Relative expression of selected lipid metabolism and PPARγ pathway proteins across the four groups. ( # p < 0.05, ## p < 0.01, ### p < 0.001 vs. CON; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. HG/PA; & p < 0.05, && p < 0.01, &&& p < 0.001 vs. HG/PA + 5% ZQC-S + g1929).
Pparγ, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pparg/PPAR+gamma+Rabbit+mAb/pmc13067941-29-190-192
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ABclonal Biotechnology antibodies against pgc1 α
The SnRNA-seq analysis of the hippocampus in aged mice after anesthesia and surgery. (A) UMAP dimensionality reduction maps of ten cell types in hippocampus; (B) Dot plot showed specific highly expressed genes in each cell type of hippocampus; (C) Secondary clustering identified four microglial subpopulations with distinct transcriptomic profiles; (D) Heatmap showed the top ten DEGs of each subpopulation; (E) Dot plot showed the expression of the marker genes in different subpopulations; (F) Pie charts showed the proportion of microglial subpopulations relative to the total microglia; (G) Bar graphs showed the relative change in the Sur group compared with the Con group, calculated as (proportion in the Sur group- proportion in the Con group)/proportion in the Con group; (H) The volcanic plot illustrated the expression of microglial <t>Ppargc1a</t> in the Sur group compare to the Con group; (I) KEGG enrichment analysis of hippocampal microglia; (J) GO enrichment analysis of hippocampal microglia; (K) Comparisons for the changes of cell-cell interactions in all pairs of cells between the Sur and Con groups. Red edges represented increased signalings in the Sur group, blue edges represented increased signalings in the Con group; (L) Comparisons for the changes of cell-cell interactions in all pairs of microglia, inhibitory neuron and excitatory neuron between the Sur and Con groups.
Antibodies Against Pgc1 α, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pparg/PGC1+alpha+Rabbit+pAb/pmc13086008-195-27-31
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93
Boster Bio pparγ
Primers for qRT-PCR analyses.
Pparγ, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pparg/Anti-PPAR+gamma+Rabbit+Monoclonal+Antibody/pmc13657433-113-50-51
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94
Novus Biologicals pparγ nbp2 22106 antibodies
Figure 3. LG100754 attenuates the binding effect of PPARα and <t>PPAR</t> γ on the CRBN promoter area. (A) U266 and MM1.R were transfected with CRBN/PGL3 firefly luciferase reported vector construct, then co-treated with PPARs agonist with LG100754 for 48 h, and luciferase bio-luminate activity was measured. (B) Bar graphs show qRT-PCR data using immunoprecipitated DNA obtained from ChIP with anti-CRBN or anti-IgG (negative control) antibodies; error bars represent SD. Results are presented as mean ± SD from at least three separate experiments. NS: not statistically significant; *: p < 0.05; **: p < 0.01.
Pparγ Nbp2 22106 Antibodies, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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92
Novus Biologicals pparg antibody
Figure 3. LG100754 attenuates the binding effect of PPARα and <t>PPAR</t> γ on the CRBN promoter area. (A) U266 and MM1.R were transfected with CRBN/PGL3 firefly luciferase reported vector construct, then co-treated with PPARs agonist with LG100754 for 48 h, and luciferase bio-luminate activity was measured. (B) Bar graphs show qRT-PCR data using immunoprecipitated DNA obtained from ChIP with anti-CRBN or anti-IgG (negative control) antibodies; error bars represent SD. Results are presented as mean ± SD from at least three separate experiments. NS: not statistically significant; *: p < 0.05; **: p < 0.01.
Pparg Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pparg/PPAR+gamma%2FNR1C3+Antibody+-+BSA+Free/pm39148124-99-9-17
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Image Search Results


BPZ disrupts fatty acids utilisation in human ovarian GCs. Schematic representation of fatty acids utilization and inhibitory action of Etomoxir ( A ). Oxygen consumption rate (OCR) changes post BPZ treatment in fatty acids dependency ( B ) and capacity ( C ) tests. BPZ-induced changes in fatty acids dependency, capacity and flexibility in primary GCs ( D , E , F ). Effects of BPZ on mRNA expression of fatty acids transporters, SLC27A1 ( G ) and CD36 ( H ) in HGrC1 cells. PPARA ( I ), PPARD ( J ) and PPARG ( K ) mRNA expression after BPZ treatment in primary GCs. Fatty acids uptake in primary GCs after 6 h BPZ treatment ( L ). Changes in viability post BPZ, fatty acids dependent pathway inhibitor, Etomoxir and co-treatment with both in HGrC1 cells ( M ). C, control (0.1% DMSO). Data are mean ± SD of three independent experiments. ** p ≤ 0.01; control vs. experimental group ( D – I ). Statistically significant are the mean values not sharing letters, p ≤ 0.05; pairwise comparison between each experimental group and the control ( J )

Journal: Archives of Toxicology

Article Title: Bisphenol Z at environmentally relevant dose dysregulates mitochondrial metabolism and proliferative capacity in human ovarian granulosa cells by inducing changes in metabolic substrate utilization

doi: 10.1007/s00204-025-04278-8

Figure Lengend Snippet: BPZ disrupts fatty acids utilisation in human ovarian GCs. Schematic representation of fatty acids utilization and inhibitory action of Etomoxir ( A ). Oxygen consumption rate (OCR) changes post BPZ treatment in fatty acids dependency ( B ) and capacity ( C ) tests. BPZ-induced changes in fatty acids dependency, capacity and flexibility in primary GCs ( D , E , F ). Effects of BPZ on mRNA expression of fatty acids transporters, SLC27A1 ( G ) and CD36 ( H ) in HGrC1 cells. PPARA ( I ), PPARD ( J ) and PPARG ( K ) mRNA expression after BPZ treatment in primary GCs. Fatty acids uptake in primary GCs after 6 h BPZ treatment ( L ). Changes in viability post BPZ, fatty acids dependent pathway inhibitor, Etomoxir and co-treatment with both in HGrC1 cells ( M ). C, control (0.1% DMSO). Data are mean ± SD of three independent experiments. ** p ≤ 0.01; control vs. experimental group ( D – I ). Statistically significant are the mean values not sharing letters, p ≤ 0.05; pairwise comparison between each experimental group and the control ( J )

Article Snippet: To assess the mRNA expression of glucose, fatty acids and glutamine transporters real-time PCR was performed using following genes: glucose transporter 1 (GLUT1, SLC2A1 ; Hs00892681_m1), glucose transporter 4 (GLUT4, SLC2A4 ; Hs00168966_m1), CD36 molecule ( CD36 , hs00354519_m1), solute carrier family 27 member 1 ( SLC27A1 , hs01587911_m1), solute carrier family 1 member 5 ( SLC5A1 , Hs01056542_m1) and peroxisome proliferator‐activated receptors: α ( PPARA , Hs00947536_m1), δ ( PPARD , Hs04187066_g1) and γ ( PPARG , Hs00234592_m1).

Techniques: Expressing, Control, Comparison

Fig. 5 Kaempferol modulated estrogen metabolism pathways and differentially regulates PPARG expression in EC cells of different ER subtypes. A– B HSD17B1 and HSD17B1-associated genes, such as ESRRA, PPARG, and ESR1, are involved in several estrogen metabolism pathways, such as steroid binding, 17- beta-hydroxysteroid dehydrogenase (NADP+) activity, steroid hormone biosynthesis, and regulation of hormone levels. C Kaempferol suppressed the expression of PPARG in ER-positive AN3 CA and promoted the expression of PPARG in ER-negative HEC-1-A. D–I Kaempferol suppressed the expression of PPARGC1A and ESRRA in both AN3 CA (D–F) and HEC-1-A cells (G–I), without modulating ESR1. Western blotting (D–E and G–H) and the IHC scores (F and I) confirmed the differential expression of PPARGC1A and ESRRA. Results are presented as means and SDs. Compared with the negative control, *, #P < 0.05, **, ##P < 0.01, ***, ###P < 0.001

Journal: Journal of translational medicine

Article Title: An integrated approach of network pharmacology, molecular docking, and experimental verification uncovers kaempferol as the effective modulator of HSD17B1 for treatment of endometrial cancer.

doi: 10.1186/s12967-023-04048-z

Figure Lengend Snippet: Fig. 5 Kaempferol modulated estrogen metabolism pathways and differentially regulates PPARG expression in EC cells of different ER subtypes. A– B HSD17B1 and HSD17B1-associated genes, such as ESRRA, PPARG, and ESR1, are involved in several estrogen metabolism pathways, such as steroid binding, 17- beta-hydroxysteroid dehydrogenase (NADP+) activity, steroid hormone biosynthesis, and regulation of hormone levels. C Kaempferol suppressed the expression of PPARG in ER-positive AN3 CA and promoted the expression of PPARG in ER-negative HEC-1-A. D–I Kaempferol suppressed the expression of PPARGC1A and ESRRA in both AN3 CA (D–F) and HEC-1-A cells (G–I), without modulating ESR1. Western blotting (D–E and G–H) and the IHC scores (F and I) confirmed the differential expression of PPARGC1A and ESRRA. Results are presented as means and SDs. Compared with the negative control, *, #P < 0.05, **, ##P < 0.01, ***, ###P < 0.001

Article Snippet: The whole cell lysates and tumor homogenates (50 μg) were resolved on an 8 ~ 12% SDS–polyacrylamide gel, transferred to a polyvinylidene difluoride membrane (NEN Life Sciences, Boston, MA), probed sequentially with antibodies against ESR1 (ab108398, 67 kDa), ESRRA (ab137489, 55 kDa), PPARGC1A (ab188102, 91 kDa) (Abcam, Cambridge, MA, U. S.), CASP3/p17/p19 (19677–1, 35 kDa), CASP9/p35/p10 (66169–1, 46 kDa), PPARG (16643–1, 55 kDa), HSD17B1 (25334–1, 35 kDa) (Proteintech, Wuhan, China) at 4 °C overnight, rinsed, and incubated with the goat anti-rabbit secondary antibody (Abcam, Cambridge, MA).

Techniques: Expressing, Binding Assay, Activity Assay, Western Blot, Quantitative Proteomics, Negative Control

ZQC regulates lipid metabolism via the PPARγ pathway in HG/PA-induced HepG2 cells. (A,B) Intracellular TG and T-CHO levels. (C,D) Relative expression of proteins (e.g., SREBP-1c, ACC1). (E–H) WB quantification of representative lipogenic and PPARγ pathway proteins (FASN, PPARγ, CD36, FABP4) in control, HG/PA, HG/PA + 5% ZQC-S, and HG/PA + 7.5% ZQC-S groups. (I) Representative Oil Red O staining images of lipid droplets. (J) Quantification of lipid droplet content (ORO%) in each group. (K,L) Intracellular TG and T-CHO levels. (M) WB analysis of key proteins in control, HG/PA, HG/PA + 7.5% ZQC-S, and HG/PA + 7.5% ZQC-S + GW1929 groups. (N–S) Relative expression of selected lipid metabolism and PPARγ pathway proteins across the four groups. ( # p < 0.05, ## p < 0.01, ### p < 0.001 vs. CON; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. HG/PA; & p < 0.05, && p < 0.01, &&& p < 0.001 vs. HG/PA + 5% ZQC-S + g1929).

Journal: Frontiers in Nutrition

Article Title: Zhaqu compound improves glucose and lipid metabolism in T2DM with MASLD by modulating gut microbiota and PPARγ

doi: 10.3389/fnut.2026.1775686

Figure Lengend Snippet: ZQC regulates lipid metabolism via the PPARγ pathway in HG/PA-induced HepG2 cells. (A,B) Intracellular TG and T-CHO levels. (C,D) Relative expression of proteins (e.g., SREBP-1c, ACC1). (E–H) WB quantification of representative lipogenic and PPARγ pathway proteins (FASN, PPARγ, CD36, FABP4) in control, HG/PA, HG/PA + 5% ZQC-S, and HG/PA + 7.5% ZQC-S groups. (I) Representative Oil Red O staining images of lipid droplets. (J) Quantification of lipid droplet content (ORO%) in each group. (K,L) Intracellular TG and T-CHO levels. (M) WB analysis of key proteins in control, HG/PA, HG/PA + 7.5% ZQC-S, and HG/PA + 7.5% ZQC-S + GW1929 groups. (N–S) Relative expression of selected lipid metabolism and PPARγ pathway proteins across the four groups. ( # p < 0.05, ## p < 0.01, ### p < 0.001 vs. CON; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. HG/PA; & p < 0.05, && p < 0.01, &&& p < 0.001 vs. HG/PA + 5% ZQC-S + g1929).

Article Snippet: The reagents and antibodies used were the Total Protein (TP) Assay Kit (1,000 tests, P0006, Biyuntian Biotechnology, China), Glucose Assay Kit (96 T, A154-1-1, Nanjing Jiancheng Bioengineering Institute, China), Total Cholesterol (T-CHO) Assay Kit (96 T, A111-1-1, Nanjing Jiancheng Bioengineering Institute, China), Triglyceride (TG) Assay Kit (96 T, A110-1-1, Nanjing Jiancheng Bioengineering Institute, China), Sequencing Reagent Kit (NovaSeq 6,000 SP Reagent Kit V1.5, Illumina, USA), RNA Mini Kit (Qiagen, Germany), DMEM High Glucose Medium (PM150210, Procell, China), Trypsin (S310JV, Shanghai Yuanpei, China), Fetal Bovine Serum (C04001-500, Vivacell, China), Double Antibody (S110JV, Shanghai Yuanpei, China), PPARγ agonist (HY-146480, MCE, USA), Palmitic acid (H8780, Solarbio, China), Oil Red O staining kit (G1262, Solarbio, China), 2-NBDG fluorescent probe (HY-116215, MCE, USA), BCA protein concentration assay kit (BL521C, Biosharp, China), SDS-PAGE Protein Loading Buffer (5×) (BL502A, Biosharp, China), ECL Chemiluminescent Substrate (BL520B, Biosharp, China), Western Blot & IP Cell Lysis Buffer (P0013, Beyotime, China), PBS Buffer ( PB180327 , Procell, China), and the primary antibodies β -Microtubulin (AC026, Abclonal, China), PEPCK (ET7107-29, Huabio, China), G6Pase (A21168, Abclonal, China), GLUT2 (A12307, Abclonal, China), SREBP-1C (ER1917-19, Huabio, China), ACC1 (ET1609-77, Huabio, China), FASN (R1706-8, Huabio, China), PPARγ (A19676, Abclonal, China), CD36 (ET1701-24, Huabio, China), and FABP4 (ET1703-98, Huabio, China).

Techniques: Expressing, Control, Staining

The SnRNA-seq analysis of the hippocampus in aged mice after anesthesia and surgery. (A) UMAP dimensionality reduction maps of ten cell types in hippocampus; (B) Dot plot showed specific highly expressed genes in each cell type of hippocampus; (C) Secondary clustering identified four microglial subpopulations with distinct transcriptomic profiles; (D) Heatmap showed the top ten DEGs of each subpopulation; (E) Dot plot showed the expression of the marker genes in different subpopulations; (F) Pie charts showed the proportion of microglial subpopulations relative to the total microglia; (G) Bar graphs showed the relative change in the Sur group compared with the Con group, calculated as (proportion in the Sur group- proportion in the Con group)/proportion in the Con group; (H) The volcanic plot illustrated the expression of microglial Ppargc1a in the Sur group compare to the Con group; (I) KEGG enrichment analysis of hippocampal microglia; (J) GO enrichment analysis of hippocampal microglia; (K) Comparisons for the changes of cell-cell interactions in all pairs of cells between the Sur and Con groups. Red edges represented increased signalings in the Sur group, blue edges represented increased signalings in the Con group; (L) Comparisons for the changes of cell-cell interactions in all pairs of microglia, inhibitory neuron and excitatory neuron between the Sur and Con groups.

Journal: International Journal of Biological Sciences

Article Title: Microglial PGC-1α alleviates synaptic damage and cognitive impairments following anesthesia and surgery by suppressing excessive synaptic pruning in aged mice

doi: 10.7150/ijbs.121472

Figure Lengend Snippet: The SnRNA-seq analysis of the hippocampus in aged mice after anesthesia and surgery. (A) UMAP dimensionality reduction maps of ten cell types in hippocampus; (B) Dot plot showed specific highly expressed genes in each cell type of hippocampus; (C) Secondary clustering identified four microglial subpopulations with distinct transcriptomic profiles; (D) Heatmap showed the top ten DEGs of each subpopulation; (E) Dot plot showed the expression of the marker genes in different subpopulations; (F) Pie charts showed the proportion of microglial subpopulations relative to the total microglia; (G) Bar graphs showed the relative change in the Sur group compared with the Con group, calculated as (proportion in the Sur group- proportion in the Con group)/proportion in the Con group; (H) The volcanic plot illustrated the expression of microglial Ppargc1a in the Sur group compare to the Con group; (I) KEGG enrichment analysis of hippocampal microglia; (J) GO enrichment analysis of hippocampal microglia; (K) Comparisons for the changes of cell-cell interactions in all pairs of cells between the Sur and Con groups. Red edges represented increased signalings in the Sur group, blue edges represented increased signalings in the Con group; (L) Comparisons for the changes of cell-cell interactions in all pairs of microglia, inhibitory neuron and excitatory neuron between the Sur and Con groups.

Article Snippet: Membranes were washed three times with TBST and blocked with 2% BSA for 2 h at room temperature, followed by overnight incubation at 4 °C with primary antibodies against PGC1-α (A12348, ABclonal), NRF-1 (A3251, ABclonal), TFAM (A3173, ABclonal), COX IV (11242-1-AP, Proteintech), ATP5A1 (14676-1-AP, Proteintech), PSD-95 (20665-1-AP, Proteintech), Synaptophysin (17785-1-AP, Proteintech), NMDAR1 (ET1703-75, HuaBio), NMDAR2A (ET1704-80, HuaBio), NMDAR2B (HA722284, HuaBio), and β-actin (R1207-1, HuaBio).

Techniques: Expressing, Marker

Primers for qRT-PCR analyses.

Journal: Frontiers in Genetics

Article Title: HOTAIR regulates osteogenic–adipogenic differentiation imbalance through the miR-217/DKK1-mediated Wnt/β-catenin pathway in SONFH-BMSCs

doi: 10.3389/fgene.2026.1917162

Figure Lengend Snippet: Primers for qRT-PCR analyses.

Article Snippet: The membranes were blocked with 5% non-fat milk in Tris-buffered saline with 0.1% Tween-20 (TBST) for 1 h at room temperature and then incubated overnight at 4 °C with primary antibodies targeting Osterix (Boster, Cat. No. M02077, 1:1,000), BMP2 (Boster, Cat. No. BM4960, 1:1,000), RUNX2 (Boster, Cat. No. BM4700, 1:1,000), PPARγ (Boster, Cat. No. M00449-2, 1:1,000), C/EBPα (Boster, Cat. No. A00386-1, 1:1,000), Adipsin (Boster, Cat. No. M01134, 1:1,000), DKK1 (Boster, Cat. No. A09360-1, 1:1,000), OCT4 (Abmart, Cat. No. T55781 , 1:10,000), β-catenin (Abmart, Cat. No. M24002 , 1:10,000), and β-actin (Boster, Cat. No. BM3873, 1:10,000).

Techniques: Sequencing

HOTAIR silencing inhibits adipogenic differentiation of SONFH-BMSCs in vitro . (A) Oil Red O staining of FNF-derived control BMSCs (NC), untreated SONFH-BMSCs, SONFH si-NC, and SONFH si-HOTAIR groups at days 7 and 14. (B) Quantitative analysis of Oil Red O staining at days 7 and 14. (C) qRT-PCR analysis of PPARγ, C/EBPα, and Adipsin mRNA levels. Expression was normalized to GAPDH and is shown compared with untreated SONFH-BMSCs and si-NC controls. (D) Western blot analysis of PPARγ, C/EBPα, and Adipsin. Data are presented as mean ± SD from three independent biological replicates using BMSCs from independent donors, with three technical replicates per experiment. (*P < 0.05; **P < 0.01; ***P < 0.001).

Journal: Frontiers in Genetics

Article Title: HOTAIR regulates osteogenic–adipogenic differentiation imbalance through the miR-217/DKK1-mediated Wnt/β-catenin pathway in SONFH-BMSCs

doi: 10.3389/fgene.2026.1917162

Figure Lengend Snippet: HOTAIR silencing inhibits adipogenic differentiation of SONFH-BMSCs in vitro . (A) Oil Red O staining of FNF-derived control BMSCs (NC), untreated SONFH-BMSCs, SONFH si-NC, and SONFH si-HOTAIR groups at days 7 and 14. (B) Quantitative analysis of Oil Red O staining at days 7 and 14. (C) qRT-PCR analysis of PPARγ, C/EBPα, and Adipsin mRNA levels. Expression was normalized to GAPDH and is shown compared with untreated SONFH-BMSCs and si-NC controls. (D) Western blot analysis of PPARγ, C/EBPα, and Adipsin. Data are presented as mean ± SD from three independent biological replicates using BMSCs from independent donors, with three technical replicates per experiment. (*P < 0.05; **P < 0.01; ***P < 0.001).

Article Snippet: The membranes were blocked with 5% non-fat milk in Tris-buffered saline with 0.1% Tween-20 (TBST) for 1 h at room temperature and then incubated overnight at 4 °C with primary antibodies targeting Osterix (Boster, Cat. No. M02077, 1:1,000), BMP2 (Boster, Cat. No. BM4960, 1:1,000), RUNX2 (Boster, Cat. No. BM4700, 1:1,000), PPARγ (Boster, Cat. No. M00449-2, 1:1,000), C/EBPα (Boster, Cat. No. A00386-1, 1:1,000), Adipsin (Boster, Cat. No. M01134, 1:1,000), DKK1 (Boster, Cat. No. A09360-1, 1:1,000), OCT4 (Abmart, Cat. No. T55781 , 1:10,000), β-catenin (Abmart, Cat. No. M24002 , 1:10,000), and β-actin (Boster, Cat. No. BM3873, 1:10,000).

Techniques: In Vitro, Staining, Derivative Assay, Control, Analysis, Quantitative RT-PCR, Expressing, Western Blot

Figure 3. LG100754 attenuates the binding effect of PPARα and PPAR γ on the CRBN promoter area. (A) U266 and MM1.R were transfected with CRBN/PGL3 firefly luciferase reported vector construct, then co-treated with PPARs agonist with LG100754 for 48 h, and luciferase bio-luminate activity was measured. (B) Bar graphs show qRT-PCR data using immunoprecipitated DNA obtained from ChIP with anti-CRBN or anti-IgG (negative control) antibodies; error bars represent SD. Results are presented as mean ± SD from at least three separate experiments. NS: not statistically significant; *: p < 0.05; **: p < 0.01.

Journal: Cells

Article Title: RXR Agonists Enhance Lenalidomide Anti-Myeloma Activity and T Cell Functions while Retaining Glucose-Lowering Effect.

doi: 10.3390/cells12151993

Figure Lengend Snippet: Figure 3. LG100754 attenuates the binding effect of PPARα and PPAR γ on the CRBN promoter area. (A) U266 and MM1.R were transfected with CRBN/PGL3 firefly luciferase reported vector construct, then co-treated with PPARs agonist with LG100754 for 48 h, and luciferase bio-luminate activity was measured. (B) Bar graphs show qRT-PCR data using immunoprecipitated DNA obtained from ChIP with anti-CRBN or anti-IgG (negative control) antibodies; error bars represent SD. Results are presented as mean ± SD from at least three separate experiments. NS: not statistically significant; *: p < 0.05; **: p < 0.01.

Article Snippet: The PPARβ/δ (NBP2-22468) and PPARγ (NBP2-22106) antibodies were obtained from Novus Biologicals, LLC. (Littleton, CO, USA).

Techniques: Binding Assay, Transfection, Luciferase, Plasmid Preparation, Construct, Activity Assay, Quantitative RT-PCR, Immunoprecipitation, Negative Control