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astrapterocarpan (MedChemExpress)

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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 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/hy-n2484/Methylnissolin/pmc12613080-72-14-19
Average 94 stars, based on 4 article reviews

astrapterocarpan - by Bioz Stars, 2026-10

94/100 stars

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1) Product Images from "Jinbei Decoction Attenuates LPS‐Induced Acute Lung Injury via Suppression of TRAF6‐Dependent Inflammatory Response in Macrophage"

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

Journal: Journal of Cellular and Molecular Medicine

doi: 10.1111/jcmm.70944

Figure Legend 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.

Techniques Used: 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.

Figure Legend 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.

Techniques Used: 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.

Figure Legend 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.

Techniques Used: 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.

Figure Legend 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.

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

Membrane:

Article Title: Uncovering the mechanism of Buyang Huanwu Decoction in regulating mitochondrial dysfunction to alleviate atherosclerosis: BTK, PREPL, and P2RX7 proteins play key roles.
Article Snippet: The purpose of this study was to uncover key target proteins and corresponding active ingredients of Buxue Huanwu Decoction (BYHWD) on improving mitochondrial function to alleviate atherosclerosis (AS) via construction of a novel strategy based on in silico virtual screening, UHPLC-Q-TOF-MS/MS, and experimental verification.. Firstly, 57 compounds of BYHWD were identified using UHPLC-Q-TOF-MS/MS technology, followed by the selection of 13 candidate compounds using Druggability predictions.. Subsequently, a combination of differentially expressed genes (DEGs), weighted gene co-expression network analysis (WGCNA), and machine learning methods were employed to identify three hub genes associated with mitochondrial function and AS, including BTK, P2RX7 and PREPL.

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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

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.

Techniques: Binding Assay

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.

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

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.

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

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astrapterocarpan (MedChemExpress)

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1) Product Images from "Jinbei Decoction Attenuates LPS‐Induced Acute Lung Injury via Suppression of TRAF6‐Dependent Inflammatory Response in Macrophage"

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