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Roles of A 2b R in ADO-mediated activation of the cAMP/PKA/CREB pathway in primary BMSCs. ( A ) Principal component analysis (PCA) of RNA-seq data from primary BMSCs treated with Dex or Dex + ADO. ( B ) The volcano plot presented the differentially expressed genes (DEGs) as determined by RNA-Seq in primary BMSCs treated with Dex or Dex + ADO. ( C ) Gene Ontology (GO) enrichment analysis in the biological process category for DEGs as determined by RNA-Seq in primary BMSCs treated with Dex, or Dex + ADO. ( D ) The molecular docking of ADO with mus musculus A 1 R, A 2a R, A 2b R, and A 3 R proteins. ADO is displayed in Cyan. The surrounding residues in the binding pocket are shown in green (forming a non-hydrogen bond with ADO) or magenta (forming a hydrogen bond with ADO). The hydrogen bond is labeled as yellow dashed lines. The backbone of the receptor is depicted as gray. ( E ) RT-qPCR analysis of the mRNA levels of Adora1 , Adora2a , Adora2b , and Adora3 in primary BMSCs treated with vehicle, Dex, or Dex + ADO. ( F ) RT-qPCR analysis for the expression of Runx2 in primary BMSCs of different groups. (G) Gene Set Enrichment Analysis (GSEA) plot showing the differentially expressed pathway (cAMP) between the Dex group and the Dex + ADO group as indicated by Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. ( H ) Western blot validation for the knockdown deficiency of A 2b R after transfection with si Adora2b . ( I ) <t>ELISA</t> analysis for the <t>relative</t> <t>intracellular</t> cAMP levels in BMSCs of different groups. ( J ) Western blot and quantification for the expression of PKA, p-PKA, CREB, and p-CREB in primary BMSCs. ( K ) Representative images and quantitative analysis of Alizarin Red S staining for mineralization deposit in primary BMSCs of different groups under osteogenic conditions. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ns p > 0.05, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bar: 200 μm (K).
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Roles of A 2b R in ADO-mediated activation of the cAMP/PKA/CREB pathway in primary BMSCs. ( A ) Principal component analysis (PCA) of RNA-seq data from primary BMSCs treated with Dex or Dex + ADO. ( B ) The volcano plot presented the differentially expressed genes (DEGs) as determined by RNA-Seq in primary BMSCs treated with Dex or Dex + ADO. ( C ) Gene Ontology (GO) enrichment analysis in the biological process category for DEGs as determined by RNA-Seq in primary BMSCs treated with Dex, or Dex + ADO. ( D ) The molecular docking of ADO with mus musculus A 1 R, A 2a R, A 2b R, and A 3 R proteins. ADO is displayed in Cyan. The surrounding residues in the binding pocket are shown in green (forming a non-hydrogen bond with ADO) or magenta (forming a hydrogen bond with ADO). The hydrogen bond is labeled as yellow dashed lines. The backbone of the receptor is depicted as gray. ( E ) RT-qPCR analysis of the mRNA levels of Adora1 , Adora2a , Adora2b , and Adora3 in primary BMSCs treated with vehicle, Dex, or Dex + ADO. ( F ) RT-qPCR analysis for the expression of Runx2 in primary BMSCs of different groups. (G) Gene Set Enrichment Analysis (GSEA) plot showing the differentially expressed pathway (cAMP) between the Dex group and the Dex + ADO group as indicated by Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. ( H ) Western blot validation for the knockdown deficiency of A 2b R after transfection with si Adora2b . ( I ) <t>ELISA</t> analysis for the <t>relative</t> <t>intracellular</t> cAMP levels in BMSCs of different groups. ( J ) Western blot and quantification for the expression of PKA, p-PKA, CREB, and p-CREB in primary BMSCs. ( K ) Representative images and quantitative analysis of Alizarin Red S staining for mineralization deposit in primary BMSCs of different groups under osteogenic conditions. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ns p > 0.05, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bar: 200 μm (K).
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Pharmed Pharmaceuticals e purpurea hydroalcoholic extract
Comparison of nitric oxide (NO, A): malondialdehyde (MDA, B) and telomere length (C) between control and two concentrations of <t>Echinacea</t> <t>purpurea</t> (E0.25: Echinacea 0.25%; E0.75: Echinacea 0.75%) groups. P < 0.05 is statistically considered significant.
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Roles of A 2b R in ADO-mediated activation of the cAMP/PKA/CREB pathway in primary BMSCs. ( A ) Principal component analysis (PCA) of RNA-seq data from primary BMSCs treated with Dex or Dex + ADO. ( B ) The volcano plot presented the differentially expressed genes (DEGs) as determined by RNA-Seq in primary BMSCs treated with Dex or Dex + ADO. ( C ) Gene Ontology (GO) enrichment analysis in the biological process category for DEGs as determined by RNA-Seq in primary BMSCs treated with Dex, or Dex + ADO. ( D ) The molecular docking of ADO with mus musculus A 1 R, A 2a R, A 2b R, and A 3 R proteins. ADO is displayed in Cyan. The surrounding residues in the binding pocket are shown in green (forming a non-hydrogen bond with ADO) or magenta (forming a hydrogen bond with ADO). The hydrogen bond is labeled as yellow dashed lines. The backbone of the receptor is depicted as gray. ( E ) RT-qPCR analysis of the mRNA levels of Adora1 , Adora2a , Adora2b , and Adora3 in primary BMSCs treated with vehicle, Dex, or Dex + ADO. ( F ) RT-qPCR analysis for the expression of Runx2 in primary BMSCs of different groups. (G) Gene Set Enrichment Analysis (GSEA) plot showing the differentially expressed pathway (cAMP) between the Dex group and the Dex + ADO group as indicated by Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. ( H ) Western blot validation for the knockdown deficiency of A 2b R after transfection with si Adora2b . ( I ) ELISA analysis for the relative intracellular cAMP levels in BMSCs of different groups. ( J ) Western blot and quantification for the expression of PKA, p-PKA, CREB, and p-CREB in primary BMSCs. ( K ) Representative images and quantitative analysis of Alizarin Red S staining for mineralization deposit in primary BMSCs of different groups under osteogenic conditions. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ns p > 0.05, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bar: 200 μm (K).

Journal: Bioactive Materials

Article Title: Screening of a quinonoid compounds library identifies decylubiquinone as an antioxidant and anti-apoptotic agent against glucocorticoid-induced osteoporosis via CD39/CD73/adenosine axis

doi: 10.1016/j.bioactmat.2026.03.062

Figure Lengend Snippet: Roles of A 2b R in ADO-mediated activation of the cAMP/PKA/CREB pathway in primary BMSCs. ( A ) Principal component analysis (PCA) of RNA-seq data from primary BMSCs treated with Dex or Dex + ADO. ( B ) The volcano plot presented the differentially expressed genes (DEGs) as determined by RNA-Seq in primary BMSCs treated with Dex or Dex + ADO. ( C ) Gene Ontology (GO) enrichment analysis in the biological process category for DEGs as determined by RNA-Seq in primary BMSCs treated with Dex, or Dex + ADO. ( D ) The molecular docking of ADO with mus musculus A 1 R, A 2a R, A 2b R, and A 3 R proteins. ADO is displayed in Cyan. The surrounding residues in the binding pocket are shown in green (forming a non-hydrogen bond with ADO) or magenta (forming a hydrogen bond with ADO). The hydrogen bond is labeled as yellow dashed lines. The backbone of the receptor is depicted as gray. ( E ) RT-qPCR analysis of the mRNA levels of Adora1 , Adora2a , Adora2b , and Adora3 in primary BMSCs treated with vehicle, Dex, or Dex + ADO. ( F ) RT-qPCR analysis for the expression of Runx2 in primary BMSCs of different groups. (G) Gene Set Enrichment Analysis (GSEA) plot showing the differentially expressed pathway (cAMP) between the Dex group and the Dex + ADO group as indicated by Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. ( H ) Western blot validation for the knockdown deficiency of A 2b R after transfection with si Adora2b . ( I ) ELISA analysis for the relative intracellular cAMP levels in BMSCs of different groups. ( J ) Western blot and quantification for the expression of PKA, p-PKA, CREB, and p-CREB in primary BMSCs. ( K ) Representative images and quantitative analysis of Alizarin Red S staining for mineralization deposit in primary BMSCs of different groups under osteogenic conditions. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ns p > 0.05, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bar: 200 μm (K).

Article Snippet: The intracellular cAMP level was examined by using a cAMP ELISA Kit (E-EL-0056, Elabscience, Wuhan, China) according to the manufacturer's instructions.

Techniques: Activation Assay, RNA Sequencing, Binding Assay, Labeling, Quantitative RT-PCR, Expressing, Western Blot, Biomarker Discovery, Knockdown, Transfection, Enzyme-linked Immunosorbent Assay, Staining, In Vitro

Comparison of nitric oxide (NO, A): malondialdehyde (MDA, B) and telomere length (C) between control and two concentrations of Echinacea purpurea (E0.25: Echinacea 0.25%; E0.75: Echinacea 0.75%) groups. P < 0.05 is statistically considered significant.

Journal: Veterinary and Animal Science

Article Title: Effect of Echinacea purpurea on cytokine gene expression (IL10, IL1β, TNFα, IFNγ), telomere length, lipid peroxidation, and nitric oxide in broilers reared at high altitude

doi: 10.1016/j.vas.2026.100675

Figure Lengend Snippet: Comparison of nitric oxide (NO, A): malondialdehyde (MDA, B) and telomere length (C) between control and two concentrations of Echinacea purpurea (E0.25: Echinacea 0.25%; E0.75: Echinacea 0.75%) groups. P < 0.05 is statistically considered significant.

Article Snippet: The E. purpurea hydroalcoholic extract (Raha Exir Pharmed Co., Iran) was thoroughly mixed into the basal diet at the specified inclusion rates (0.25% or 0.75%).

Techniques: Comparison, Control

Comparison of cytokine gene expression (A: IFNγ; B: IL10; C: IL1β, D: TNFα) between control and two concentrations of Echinacea purpurea (E0.25: Echinacea 0.25%; E0.75: Echinacea 0.75%) groups. P < 0.05 is statistically considered significant.

Journal: Veterinary and Animal Science

Article Title: Effect of Echinacea purpurea on cytokine gene expression (IL10, IL1β, TNFα, IFNγ), telomere length, lipid peroxidation, and nitric oxide in broilers reared at high altitude

doi: 10.1016/j.vas.2026.100675

Figure Lengend Snippet: Comparison of cytokine gene expression (A: IFNγ; B: IL10; C: IL1β, D: TNFα) between control and two concentrations of Echinacea purpurea (E0.25: Echinacea 0.25%; E0.75: Echinacea 0.75%) groups. P < 0.05 is statistically considered significant.

Article Snippet: The E. purpurea hydroalcoholic extract (Raha Exir Pharmed Co., Iran) was thoroughly mixed into the basal diet at the specified inclusion rates (0.25% or 0.75%).

Techniques: Comparison, Gene Expression, Control

Comparison of expression of cytokine gene ratio [(IFNγ + IL1β + TNFα) / IL10] between control and two concentrations of Echinacea purpurea (E0.25: Echinacea 0.25%; E0.75: Echinacea 0.75%) groups.

Journal: Veterinary and Animal Science

Article Title: Effect of Echinacea purpurea on cytokine gene expression (IL10, IL1β, TNFα, IFNγ), telomere length, lipid peroxidation, and nitric oxide in broilers reared at high altitude

doi: 10.1016/j.vas.2026.100675

Figure Lengend Snippet: Comparison of expression of cytokine gene ratio [(IFNγ + IL1β + TNFα) / IL10] between control and two concentrations of Echinacea purpurea (E0.25: Echinacea 0.25%; E0.75: Echinacea 0.75%) groups.

Article Snippet: The E. purpurea hydroalcoholic extract (Raha Exir Pharmed Co., Iran) was thoroughly mixed into the basal diet at the specified inclusion rates (0.25% or 0.75%).

Techniques: Comparison, Expressing, Control