hy-n2484 Search Results


astrapterocarpan  (MedChemExpress)
94
MedChemExpress astrapterocarpan
Screening of the bioactive constituent of JBD. (A) Shared candidate compounds identified through CytoNCA and CytoHubba computational approaches. (B) QRT‐PCR validation demonstrating <t>astrapterocarpan's</t> most potent suppression of cytokine mRNA levels versus other candidates (10 μM; **** p < 0.0001 vs. LPS). (C, E, G, I) Immunoblotting analyses of astrapterocarpan (C), baicalin (E), chlorogenic acid (G) and wogonin (I) effects on LPS induced activation of ERK and P65. (D, F, H, J) The quantitative analyses of p‐ERK, and p‐p65 protein levels were normalised to their corresponding total protein expressions affected by astrapterocarpan (D), baicalin (F), chlorogenic acid (H) and wogonin (J). (K) ELISA quantification of LPS‐induced TNFα, IL‐6 and IL‐1β levels in PEM cells following astrapterocarpan treatment. Data were presented as mean ± SEM, n = 3; with * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
Astrapterocarpan, supplied by MedChemExpress, 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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Screening of the bioactive constituent of JBD. (A) Shared candidate compounds identified through CytoNCA and CytoHubba computational approaches. (B) QRT‐PCR validation demonstrating astrapterocarpan's most potent suppression of cytokine mRNA levels versus other candidates (10 μM; **** p < 0.0001 vs. LPS). (C, E, G, I) Immunoblotting analyses of astrapterocarpan (C), baicalin (E), chlorogenic acid (G) and wogonin (I) effects on LPS induced activation of ERK and P65. (D, F, H, J) The quantitative analyses of p‐ERK, and p‐p65 protein levels were normalised to their corresponding total protein expressions affected by astrapterocarpan (D), baicalin (F), chlorogenic acid (H) and wogonin (J). (K) ELISA quantification of LPS‐induced TNFα, IL‐6 and IL‐1β levels in PEM cells following astrapterocarpan treatment. Data were presented as mean ± SEM, n = 3; with * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Jinbei Decoction Attenuates LPS‐Induced Acute Lung Injury via Suppression of TRAF6‐Dependent Inflammatory Response in Macrophage

doi: 10.1111/jcmm.70944

Figure Lengend Snippet: Screening of the bioactive constituent of JBD. (A) Shared candidate compounds identified through CytoNCA and CytoHubba computational approaches. (B) QRT‐PCR validation demonstrating astrapterocarpan's most potent suppression of cytokine mRNA levels versus other candidates (10 μM; **** p < 0.0001 vs. LPS). (C, E, G, I) Immunoblotting analyses of astrapterocarpan (C), baicalin (E), chlorogenic acid (G) and wogonin (I) effects on LPS induced activation of ERK and P65. (D, F, H, J) The quantitative analyses of p‐ERK, and p‐p65 protein levels were normalised to their corresponding total protein expressions affected by astrapterocarpan (D), baicalin (F), chlorogenic acid (H) and wogonin (J). (K) ELISA quantification of LPS‐induced TNFα, IL‐6 and IL‐1β levels in PEM cells following astrapterocarpan treatment. Data were presented as mean ± SEM, n = 3; with * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: The compounds baicalin (HY‐N0197), wogonin (HY‐N0400), chlorogenic acid (HY‐N0055), glycyrrhizin (HY‐N0184), phenylalanine (HY‐N0215) and astrapterocarpan (HY‐N2484) were sourced from MedChemExpress.

Techniques: Quantitative RT-PCR, Biomarker Discovery, Western Blot, Activation Assay, Enzyme-linked Immunosorbent Assay

The prediction of potential binding targets of astrapterocarpan. (A) Schematic of TLR4‐MyD88‐TRAF6‐TAK1‐NF‐κB/MAPK pathway. (B) Heatmap of molecular docking binding energies (kcal/mol), demonstrating astrapterocarpan's binding affinity for the indicated proteins, including TLR4, MyD88, IRAK4, TRAF6 and TAK1. (C) Computational modelling (PyMOL) illustrating astrapterocarpan's interaction patterns with TLR4, MyD88, IRAK4 and TRAF6 residues. (D) Free energy landscape (FEL) analysis demonstrated the conformational state of the four proteins (TLR4, MyD88, IRAK4 and TRAF6) upon the compound binding, as indicated by changes in global energy distribution.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Jinbei Decoction Attenuates LPS‐Induced Acute Lung Injury via Suppression of TRAF6‐Dependent Inflammatory Response in Macrophage

doi: 10.1111/jcmm.70944

Figure Lengend Snippet: The prediction of potential binding targets of astrapterocarpan. (A) Schematic of TLR4‐MyD88‐TRAF6‐TAK1‐NF‐κB/MAPK pathway. (B) Heatmap of molecular docking binding energies (kcal/mol), demonstrating astrapterocarpan's binding affinity for the indicated proteins, including TLR4, MyD88, IRAK4, TRAF6 and TAK1. (C) Computational modelling (PyMOL) illustrating astrapterocarpan's interaction patterns with TLR4, MyD88, IRAK4 and TRAF6 residues. (D) Free energy landscape (FEL) analysis demonstrated the conformational state of the four proteins (TLR4, MyD88, IRAK4 and TRAF6) upon the compound binding, as indicated by changes in global energy distribution.

Article Snippet: The compounds baicalin (HY‐N0197), wogonin (HY‐N0400), chlorogenic acid (HY‐N0055), glycyrrhizin (HY‐N0184), phenylalanine (HY‐N0215) and astrapterocarpan (HY‐N2484) were sourced from MedChemExpress.

Techniques: Binding Assay

Astrapterocarpan specifically interacts with TRAF6. (A, C) Cellular thermal shift assays (CETSA) of TRAF6 in (A) RAW264.7 macrophages and (C) PEMs treated with or without Astrapterocarpan (20 μM). Lysates were subjected to temperature gradient followed by western blot analysis (* p < 0.05, ** p < 0.01 vs. untreated controls). (B, D) The quantitative analyses of TLR4, MyD88, IRAK4 and TRAF6 protein levels were performed by calculating the grayscale values, which were normalised to the values obtained under the condition of 37°C for both RAW264.7 (B) and PEM cells (D). (E–H) Luciferase reporter plasmids containing the NF‐κB promoter were co‐transfected with expression plasmids encoding the indicated proteins, including MyD88 (E), IRAK4 (F), TRAF6 (G) and TAK1 (H), into RAW264.7 cells. After a 24‐h incubation period post‐transfection, the cells were collected and luciferase activity was assessed using a luciferase reporter assay kit. (I) Alveolar macrophages were isolated from LPS‐induced mice that had been administered different doses of JBD via intragastric gavage to evaluate the expression levels of the indicated proteins, including TLR4, MyD88, IRAK4 and TRAF6. (J) Quantitative analyses of TLR4, MyD88, IRAK4 and TRAF6 protein levels were normalised relative to GAPDH expression. Astraptn: Astrapterocarpan. * p < 0.05, *** p < 0.001, **** p < 0.0001.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Jinbei Decoction Attenuates LPS‐Induced Acute Lung Injury via Suppression of TRAF6‐Dependent Inflammatory Response in Macrophage

doi: 10.1111/jcmm.70944

Figure Lengend Snippet: Astrapterocarpan specifically interacts with TRAF6. (A, C) Cellular thermal shift assays (CETSA) of TRAF6 in (A) RAW264.7 macrophages and (C) PEMs treated with or without Astrapterocarpan (20 μM). Lysates were subjected to temperature gradient followed by western blot analysis (* p < 0.05, ** p < 0.01 vs. untreated controls). (B, D) The quantitative analyses of TLR4, MyD88, IRAK4 and TRAF6 protein levels were performed by calculating the grayscale values, which were normalised to the values obtained under the condition of 37°C for both RAW264.7 (B) and PEM cells (D). (E–H) Luciferase reporter plasmids containing the NF‐κB promoter were co‐transfected with expression plasmids encoding the indicated proteins, including MyD88 (E), IRAK4 (F), TRAF6 (G) and TAK1 (H), into RAW264.7 cells. After a 24‐h incubation period post‐transfection, the cells were collected and luciferase activity was assessed using a luciferase reporter assay kit. (I) Alveolar macrophages were isolated from LPS‐induced mice that had been administered different doses of JBD via intragastric gavage to evaluate the expression levels of the indicated proteins, including TLR4, MyD88, IRAK4 and TRAF6. (J) Quantitative analyses of TLR4, MyD88, IRAK4 and TRAF6 protein levels were normalised relative to GAPDH expression. Astraptn: Astrapterocarpan. * p < 0.05, *** p < 0.001, **** p < 0.0001.

Article Snippet: The compounds baicalin (HY‐N0197), wogonin (HY‐N0400), chlorogenic acid (HY‐N0055), glycyrrhizin (HY‐N0184), phenylalanine (HY‐N0215) and astrapterocarpan (HY‐N2484) were sourced from MedChemExpress.

Techniques: Western Blot, Luciferase, Transfection, Expressing, Incubation, Activity Assay, Reporter Assay, Isolation

Astrapterocarpan attenuates LPS‐induced ALI in vivo. (A) The experimental design is illustrated as follows: Mice received pretreatment with astrapterocarpan (5/10 mg/kg) or dexamethasone (10 mg/kg) prior to LPS challenge. (B) Survival analysis showed high‐dose astrapterocarpan achieved comparable efficacy to dexamethasone in extending survival duration (48‐h observation period; n = 10 animals per group). (C) Histopathological evaluation through H&E staining (scale bars = 100 μm) revealed a dose‐responsive reduction in pulmonary injury severity. (D, E) The lung tissues were collected from LPS‐induced mice that had been administrated different doses of astrapterocarpan to evaluate the activation of ERK and p65 by western blot (D), and the quantitative analyses of p‐ERK, and p‐p65 protein levels were normalised to their corresponding total protein expressions affected by astrapterocarpan (E). (F, G) Alveolar macrophages were isolated from LPS‐induced mice that had been administered different doses of astrapterocarpan to evaluate the activation of ERK and p65 by western blot (F), and the quantitative analyses of p‐ERK, and p‐p65 protein levels were normalised to their corresponding total protein expressions affected by astrapterocarpan (G). All experimental results present mean ± SEM values from ≥ 3 independent trials, with * p < 0.05, ** p < 0.01, **** p < 0.0001.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Jinbei Decoction Attenuates LPS‐Induced Acute Lung Injury via Suppression of TRAF6‐Dependent Inflammatory Response in Macrophage

doi: 10.1111/jcmm.70944

Figure Lengend Snippet: Astrapterocarpan attenuates LPS‐induced ALI in vivo. (A) The experimental design is illustrated as follows: Mice received pretreatment with astrapterocarpan (5/10 mg/kg) or dexamethasone (10 mg/kg) prior to LPS challenge. (B) Survival analysis showed high‐dose astrapterocarpan achieved comparable efficacy to dexamethasone in extending survival duration (48‐h observation period; n = 10 animals per group). (C) Histopathological evaluation through H&E staining (scale bars = 100 μm) revealed a dose‐responsive reduction in pulmonary injury severity. (D, E) The lung tissues were collected from LPS‐induced mice that had been administrated different doses of astrapterocarpan to evaluate the activation of ERK and p65 by western blot (D), and the quantitative analyses of p‐ERK, and p‐p65 protein levels were normalised to their corresponding total protein expressions affected by astrapterocarpan (E). (F, G) Alveolar macrophages were isolated from LPS‐induced mice that had been administered different doses of astrapterocarpan to evaluate the activation of ERK and p65 by western blot (F), and the quantitative analyses of p‐ERK, and p‐p65 protein levels were normalised to their corresponding total protein expressions affected by astrapterocarpan (G). All experimental results present mean ± SEM values from ≥ 3 independent trials, with * p < 0.05, ** p < 0.01, **** p < 0.0001.

Article Snippet: The compounds baicalin (HY‐N0197), wogonin (HY‐N0400), chlorogenic acid (HY‐N0055), glycyrrhizin (HY‐N0184), phenylalanine (HY‐N0215) and astrapterocarpan (HY‐N2484) were sourced from MedChemExpress.

Techniques: In Vivo, Staining, Activation Assay, Western Blot, Isolation