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MedChemExpress brevilin a
Mechanistic insights into <t>Brevilin</t> <t>A</t> action against lung cancer. Schematic diagram summarizing the mechanisms underlying Brevilin A action against lung cancer using network pharmacology, molecular docking, and experimental validation

Mechanistic insights into <t>Brevilin</t> <t>A</t> action against lung cancer. Schematic diagram summarizing the mechanisms underlying Brevilin A action against lung cancer using network pharmacology, molecular docking, and experimental validation

Brevilin A, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/hy-n2959/Brevilin+A/pmc11151568-142-0-14
Average 93 stars, based on 7 article reviews

brevilin a - by Bioz Stars, 2026-10

93/100 stars

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1) Product Images from "Mechanistic prediction and validation of Brevilin A Therapeutic effects in Lung Cancer"

Article Title: Mechanistic prediction and validation of Brevilin A Therapeutic effects in Lung Cancer

Journal: BMC Complementary Medicine and Therapies

doi: 10.1186/s12906-024-04516-z

Mechanistic insights into Brevilin A action against lung cancer. Schematic diagram summarizing the mechanisms underlying Brevilin A action against lung cancer using network pharmacology, molecular docking, and experimental validation

Figure Legend Snippet: Mechanistic insights into Brevilin A action against lung cancer. Schematic diagram summarizing the mechanisms underlying Brevilin A action against lung cancer using network pharmacology, molecular docking, and experimental validation

Techniques Used: Biomarker Discovery

Differential gene expression analysis. (A) GEO Volcano Map and (B) GEO heatmap of the top 10 up- and down-regulated genes expression. Red and blue dots indicate up-regulated and down-regulated genes, respectively. (C) Venn diagram showing the overlap of Brevilin A-associated targets and lung cancer-related genes

Figure Legend Snippet: Differential gene expression analysis. (A) GEO Volcano Map and (B) GEO heatmap of the top 10 up- and down-regulated genes expression. Red and blue dots indicate up-regulated and down-regulated genes, respectively. (C) Venn diagram showing the overlap of Brevilin A-associated targets and lung cancer-related genes

Techniques Used: Gene Expression, Expressing

Brevilin A target pathway in lung cancer. (A) Brevilin A target-major pathway-lung cancer. (B) Distribution of key targets in the HIF-1 signaling pathway

Figure Legend Snippet: Brevilin A target pathway in lung cancer. (A) Brevilin A target-major pathway-lung cancer. (B) Distribution of key targets in the HIF-1 signaling pathway

Techniques Used:

Molecular docking results. (A) The binding mode of Brevilin A-HIF1A complex. (B) The binding mode of Brevilin A-PTEN complex. The 3D visualization is on the left, and the 2D visualization is on the right

Figure Legend Snippet: Molecular docking results. (A) The binding mode of Brevilin A-HIF1A complex. (B) The binding mode of Brevilin A-PTEN complex. The 3D visualization is on the left, and the 2D visualization is on the right

Techniques Used: Binding Assay

Figure Legend Snippet: The binding pose and energy between Brevilin A and the targets

Techniques Used: Binding Assay

Brevilin A-induced A549 cell death via targeting HIF-1α pathway. (A) The chemical structure of the Brevilin A. CCK8 assay in A549 cells treated with Brevilin A for 24 h (B) and 48 h (C) . (D) Photographs of A549 cells after treatment for 24 h and 48 h. mRNA expression levels of PTEN (E) and HIF-1α (F) in A549 cells treated with Brevilin A for 24 h. * p < 0.05, ** p < 0.01, **** p < 0.0001 versus vehicle control group

Figure Legend Snippet: Brevilin A-induced A549 cell death via targeting HIF-1α pathway. (A) The chemical structure of the Brevilin A. CCK8 assay in A549 cells treated with Brevilin A for 24 h (B) and 48 h (C) . (D) Photographs of A549 cells after treatment for 24 h and 48 h. mRNA expression levels of PTEN (E) and HIF-1α (F) in A549 cells treated with Brevilin A for 24 h. * p < 0.05, ** p < 0.01, **** p < 0.0001 versus vehicle control group

Techniques Used: CCK-8 Assay, Expressing, Control

High Performance Liquid Chromatography:

Article Title: Brevilin A suppresses lipid metabolism reprogramming in colorectal adenoma-to-adenocarcinoma sequence via the NR1D1/APOH signaling axis.
Article Snippet: Background: The adenoma-carcinoma sequence is a classic pathway for colorectal cancer (CRC) occurrence, and this pathway is associated with lipid metabolism reprogramming.. Brevilin A (Br), an extract from Centipeda minima, exhibits anticancer effects in multiple tumors.. However, its role in inhibiting the adenoma-carcinoma sequence remain unclear.

Injection:

Article Title: Entero-toxigenic Bacteroides fragilis contributes to intestinal barrier injury and colorectal cancer progression by mediating the BFT/STAT3/ZEB2 pathway
Article Snippet: .. C57BL/6 mice in the Brevilin A group were injected intraperitoneally with 0.1 ml Brevilin A (10 mg/kg; HY-N2959; MedChem Express, USA) after 1 h of strain gavage, with three cycles of 7 d each. ..

Biomarker Discovery:

Article Title: Mechanistic Prediction and validation of Brevilin A Therapeutic Effects in Lung Cancer
Article Snippet: .. 2.8 Experimental validation 2.8.1 Chemicals and reagents Brevilin A with 99.71% purity and Cell Counting Kit-8 (CCK-8) kit were obtained from MCE (MedChemExpress, shanghai, China). .. 2.8.2 Cell culture A549 cells were procured from the American Type Culture Collection (ATCC, Manassas, VA, USA) and subsequently cultivated in Dulbecco's Modi ed Eagle Medium (DMEM) supplemented with 10% fetal bovine serum (FBS).

CCK-8 Assay:

Article Title: Mechanistic prediction and validation of Brevilin A Therapeutic effects in Lung Cancer
Article Snippet: .. Brevilin A with 99.71% purity and Cell Counting Kit-8 (CCK-8) kit were obtained from MCE (MedChemExpress, shanghai, China). .. A549 cells were procured from the American Type Culture Collection (ATCC, Manassas, VA, USA) and subsequently cultivated in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% fetal bovine serum (FBS).

Concentration Assay:

Article Title: Brevilin A inhibits IL‑17A‑induced inflammation in psoriasis by modulating HSP 70
Article Snippet: Cell viability was assessed using the MTT assay (CAS no. 298-93-1; Sigma-Aldrich; Merck KGaA). .. Briefly, HaCaT cells were seeded at a density of 5×10 4 cells/well in a 96-well plate, and were treated with the indicated concentrations of brevilin A (0.625–20 μM) and/or apoptozole (CAS no. 1054543-47-3; MedChemExpress) (0.009–20 μM) at 37°C for 24 h. Each concentration of each substance was tested in triplicate wells (n=3). .. After 24 h of treatment, MTT solution (5 mg/ml) was added and the cells were incubated for an additional 4 h. Formazan crystals formed were dissolved in isopropanol, and the absorbance was measured at 570 nm using a microplate reader (SUNRISE; Tecan Group, Ltd).

Article Title: Brevilin A inhibits IL‑17A‑induced inflammation in psoriasis by modulating HSP 70.
Article Snippet: Psoriasis, which is characterized by keratinocyte hyperproliferation, presents complex management chal‐ lenges.. The heat shock protein 70 (HSP 70) family, which is essential in protein folding and stress responses, also modulates inflammation, suggesting its therapeutic potential in inflammation‐driven diseases.. The present study aimed to explore the effects of brevilin A, a natural compound known to alleviate imiquimod‐induced psoriasis, on HSP 70 expres‐ sion and proinflammatory cytokine production in HacaT cells stimulated with il‐17a. an HSP 70 inhibitor was used to determine its role in cytokine regulation, and the effect of brevilin A on skin pathology in mice was examined via immunohistochemistry and hematoxylin and eosin staining.

Image Search Results

Effects of brevilin A on cell viability and IL-17A induced IL-6 and IL-8 production in HaCaT cells. (A) HaCaT cells were treated with different doses of brevilin A (0.625, 1.25, 2.5, 5, 10 and 20 µM) or 2% DMSO for 24 h. Cell viability was measured by MTT assay. Results are presented as a percentage of control (untreated) cells. Data are expressed as mean ± SEM (n=3). *P<0.05 vs. control. (B) Concentrations of IL-6 and IL-8 in the supernatant were determined using ELISA kits. HaCaT cells were seeded at a density of 2×10 5 cells/well in a 24-well plate and were co-treated with IL-17A (100 ng/ml) and different concentrations of brevilin A (1.25, 2.5 and 5 µM) or dexamethasone (1 µg/ml). Samples were collected after 9 and 24 h of treatment. The concentrations of IL-6 and IL-8 were quantified, and results are presented as the mean ± SEM (n=3). *P<0.05 vs. IL-17A-treated group.

Journal: Molecular Medicine Reports

Article Title: Brevilin A inhibits IL‑17A‑induced inflammation in psoriasis by modulating HSP 70

doi: 10.3892/mmr.2025.13521

Figure Lengend Snippet: Effects of brevilin A on cell viability and IL-17A induced IL-6 and IL-8 production in HaCaT cells. (A) HaCaT cells were treated with different doses of brevilin A (0.625, 1.25, 2.5, 5, 10 and 20 µM) or 2% DMSO for 24 h. Cell viability was measured by MTT assay. Results are presented as a percentage of control (untreated) cells. Data are expressed as mean ± SEM (n=3). *P<0.05 vs. control. (B) Concentrations of IL-6 and IL-8 in the supernatant were determined using ELISA kits. HaCaT cells were seeded at a density of 2×10 5 cells/well in a 24-well plate and were co-treated with IL-17A (100 ng/ml) and different concentrations of brevilin A (1.25, 2.5 and 5 µM) or dexamethasone (1 µg/ml). Samples were collected after 9 and 24 h of treatment. The concentrations of IL-6 and IL-8 were quantified, and results are presented as the mean ± SEM (n=3). *P<0.05 vs. IL-17A-treated group.

Article Snippet: Briefly, HaCaT cells were seeded at a density of 5×10 4 cells/well in a 96-well plate, and were treated with the indicated concentrations of brevilin A (0.625–20 μM) and/or apoptozole (CAS no. 1054543-47-3; MedChemExpress) (0.009–20 μM) at 37°C for 24 h. Each concentration of each substance was tested in triplicate wells (n=3).

Techniques: MTT Assay, Control, Enzyme-linked Immunosorbent Assay

Brevilin A increases HSP 70 and HSP 90 expression in HaCaT cells. (A) HaCaT cells were treated with IL-17A alone (100 ng/ml), or were co-treated with IL-17A and brevilin A (5 µM) for different durations (0, 3, 6, 9, and 24 h). Expression levels of HSP 70, HSP 90 and β-actin (loading control) were detected by western blotting. Semi-quantitative analysis of (B) HSP 70 and (C) HSP 90 expression levels. The intensity of HSP 70/HSP 90 bands was normalized to β-actin and expressed as fold change relative to control (untreated) cells. (D) Western blot analysis of the expression levels of HSP 70 and HSP 90 in HaCaT cells treated with IL-17A (100 ng/ml) and various concentrations of brevilin A (1.25, 2.5 and 5 µM) for 9 h. β-actin was used as a loading control. (E) Semi-quantitative analysis of HSP 70 and HSP 90 band intensity was performed using ImageJ. The intensity of bands was normalized to β-actin and expressed as fold change relative to control (untreated) cells. (F) Western blot analysis of the expression levels of HSP 70 and HSP 90 in HaCaT cells treated with various concentrations of brevilin A (1.25, 2.5 and 5 µM) for 24 h. β-actin was used as a loading control. (G) Semiquantitative analysis of HSP 70 and HSP 90 band intensity was performed using ImageJ. The intensity of bands was normalized to β-actin and expressed as fold change relative to control (untreated) cells. (H) HaCaT cells were treated with IL-17A (100 ng/ml) alone, brevilin A (5 µM) alone, or a combination of IL-17A and brevilin A for 9 h. The secretion of IL-6 and IL-8 was measured by ELISA. (I) Brevilin A modulates the MAPK signaling pathway in IL-17A-treated cells. Western blot analysis was performed to assess the phosphorylation levels of SAPK/JNK, ERK and p38 MAPK after treatment with IL-17A (100 ng/ml) and different concentrations of brevilin A (1.25, 2.5 and 5 µM) for 9 h. Total SAPK/JNK, ERK and p38 protein levels were used as controls, and β-actin served as the loading control. Semi-quantification of p-SAPK/JNK, p-ERK and p-p38 was normalized to total protein levels and presented as a percentage of the control group. Data are presented as the mean ± SEM (n=3). *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 vs. control or as indicated. HSP, heat shock protein; p-, phosphorylated.

Journal: Molecular Medicine Reports

Article Title: Brevilin A inhibits IL‑17A‑induced inflammation in psoriasis by modulating HSP 70

doi: 10.3892/mmr.2025.13521

Figure Lengend Snippet: Brevilin A increases HSP 70 and HSP 90 expression in HaCaT cells. (A) HaCaT cells were treated with IL-17A alone (100 ng/ml), or were co-treated with IL-17A and brevilin A (5 µM) for different durations (0, 3, 6, 9, and 24 h). Expression levels of HSP 70, HSP 90 and β-actin (loading control) were detected by western blotting. Semi-quantitative analysis of (B) HSP 70 and (C) HSP 90 expression levels. The intensity of HSP 70/HSP 90 bands was normalized to β-actin and expressed as fold change relative to control (untreated) cells. (D) Western blot analysis of the expression levels of HSP 70 and HSP 90 in HaCaT cells treated with IL-17A (100 ng/ml) and various concentrations of brevilin A (1.25, 2.5 and 5 µM) for 9 h. β-actin was used as a loading control. (E) Semi-quantitative analysis of HSP 70 and HSP 90 band intensity was performed using ImageJ. The intensity of bands was normalized to β-actin and expressed as fold change relative to control (untreated) cells. (F) Western blot analysis of the expression levels of HSP 70 and HSP 90 in HaCaT cells treated with various concentrations of brevilin A (1.25, 2.5 and 5 µM) for 24 h. β-actin was used as a loading control. (G) Semiquantitative analysis of HSP 70 and HSP 90 band intensity was performed using ImageJ. The intensity of bands was normalized to β-actin and expressed as fold change relative to control (untreated) cells. (H) HaCaT cells were treated with IL-17A (100 ng/ml) alone, brevilin A (5 µM) alone, or a combination of IL-17A and brevilin A for 9 h. The secretion of IL-6 and IL-8 was measured by ELISA. (I) Brevilin A modulates the MAPK signaling pathway in IL-17A-treated cells. Western blot analysis was performed to assess the phosphorylation levels of SAPK/JNK, ERK and p38 MAPK after treatment with IL-17A (100 ng/ml) and different concentrations of brevilin A (1.25, 2.5 and 5 µM) for 9 h. Total SAPK/JNK, ERK and p38 protein levels were used as controls, and β-actin served as the loading control. Semi-quantification of p-SAPK/JNK, p-ERK and p-p38 was normalized to total protein levels and presented as a percentage of the control group. Data are presented as the mean ± SEM (n=3). *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 vs. control or as indicated. HSP, heat shock protein; p-, phosphorylated.

Techniques: Expressing, Control, Western Blot, Enzyme-linked Immunosorbent Assay, Phospho-proteomics

Brevilin A reduces IMQ-induced skin inflammation, decreases IL-6 expression and enhances HSP 70 expression in a mouse model of psoriasis. Briefly, 8-week-old BALB/c mice (n=5/group) with IMQ-induced psoriasis were treated with brevilin A (5, 10 and 20 mg/kg) or dexamethasone (1 mg/kg) by intraperitoneal injection for 5 consecutive days. (A) Representative images of the skin on the backs of mice showed improvement in erythema and scaling in brevilin A- and dexamethasone-treated groups compared with the vehicle control. (B) Skin pathology was assessed using hematoxylin and eosin staining (×400 magnification). Representative images show the degree of epithelial hyperproliferation and immune cell infiltration, with immune cells indicated by red arrows. Scale bar=20 µm. (C) IHC staining of HSP 70 showed increased expression in brevilin A-treated groups, with the highest expression observed at 20 mg/kg. Scale bar=50 µm; ×200 magnification. (D) IHC staining of IL-6 revealed reduced expression in brevilin A-treated groups, suggesting its anti-inflammatory effects. Scale bar=50 µm; ×200 magnification. (E) IHC staining of HSP 90 showed increased expression in brevilin A-treated groups, with the highest expression observed at 20 mg/kg. Scale bar=50 µm; ×200 magnification. (F) Semi-quantification of HSP 70, IL-6 and HSP 90 staining intensity are presented as the mean ± SEM. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. IHC, immunohistochemistry; IMQ, imiquimod

Journal: Molecular Medicine Reports

Article Title: Brevilin A inhibits IL‑17A‑induced inflammation in psoriasis by modulating HSP 70

doi: 10.3892/mmr.2025.13521

Figure Lengend Snippet: Brevilin A reduces IMQ-induced skin inflammation, decreases IL-6 expression and enhances HSP 70 expression in a mouse model of psoriasis. Briefly, 8-week-old BALB/c mice (n=5/group) with IMQ-induced psoriasis were treated with brevilin A (5, 10 and 20 mg/kg) or dexamethasone (1 mg/kg) by intraperitoneal injection for 5 consecutive days. (A) Representative images of the skin on the backs of mice showed improvement in erythema and scaling in brevilin A- and dexamethasone-treated groups compared with the vehicle control. (B) Skin pathology was assessed using hematoxylin and eosin staining (×400 magnification). Representative images show the degree of epithelial hyperproliferation and immune cell infiltration, with immune cells indicated by red arrows. Scale bar=20 µm. (C) IHC staining of HSP 70 showed increased expression in brevilin A-treated groups, with the highest expression observed at 20 mg/kg. Scale bar=50 µm; ×200 magnification. (D) IHC staining of IL-6 revealed reduced expression in brevilin A-treated groups, suggesting its anti-inflammatory effects. Scale bar=50 µm; ×200 magnification. (E) IHC staining of HSP 90 showed increased expression in brevilin A-treated groups, with the highest expression observed at 20 mg/kg. Scale bar=50 µm; ×200 magnification. (F) Semi-quantification of HSP 70, IL-6 and HSP 90 staining intensity are presented as the mean ± SEM. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. IHC, immunohistochemistry; IMQ, imiquimod

Techniques: Expressing, Injection, Control, Staining, Immunohistochemistry

Apoptozole neutralizes the effects of brevilin A on decreasing IL-17A-induced IL-6 and IL-8 levels. HaCaT cells were seeded at a density of 2×10 5 cells/well in a 24-well plate, and were co-treated with IL-17A (100 ng/ml), either brevilin A (5 µM) and different concentrations of apoptozole (1.25, 2.5 and 5 µM) for 9 and 24 h. Levels of IL-6 and IL-8 were measured by ELISA. Data are presented as the mean ± SEM (n=3). *P<0.05 vs. IL-17A-treated group; # P<0.05 vs. IL-17A + brevilin A co-treated group.

Journal: Molecular Medicine Reports

Article Title: Brevilin A inhibits IL‑17A‑induced inflammation in psoriasis by modulating HSP 70

doi: 10.3892/mmr.2025.13521

Figure Lengend Snippet: Apoptozole neutralizes the effects of brevilin A on decreasing IL-17A-induced IL-6 and IL-8 levels. HaCaT cells were seeded at a density of 2×10 5 cells/well in a 24-well plate, and were co-treated with IL-17A (100 ng/ml), either brevilin A (5 µM) and different concentrations of apoptozole (1.25, 2.5 and 5 µM) for 9 and 24 h. Levels of IL-6 and IL-8 were measured by ELISA. Data are presented as the mean ± SEM (n=3). *P<0.05 vs. IL-17A-treated group; # P<0.05 vs. IL-17A + brevilin A co-treated group.

Techniques: Enzyme-linked Immunosorbent Assay

Effects of brevilin A treatment on anti-inflammatory cytokines were reversed by apoptozole treatment. HaCaT cells were seeded at a density of 2×10 5 cells/well in a 24-well plate, and were co-treated with IL-17A (100 ng/ml), brevilin A (1.25, 2.5 and 5 µM) and apoptozole (5 µM). Samples were collected after 9 and 24 h of treatment. Levels of IL-6 and IL-8 were measured by ELISA. Data are presented as the mean ± SEM (n=3). *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001.

Journal: Molecular Medicine Reports

Article Title: Brevilin A inhibits IL‑17A‑induced inflammation in psoriasis by modulating HSP 70

doi: 10.3892/mmr.2025.13521

Figure Lengend Snippet: Effects of brevilin A treatment on anti-inflammatory cytokines were reversed by apoptozole treatment. HaCaT cells were seeded at a density of 2×10 5 cells/well in a 24-well plate, and were co-treated with IL-17A (100 ng/ml), brevilin A (1.25, 2.5 and 5 µM) and apoptozole (5 µM). Samples were collected after 9 and 24 h of treatment. Levels of IL-6 and IL-8 were measured by ELISA. Data are presented as the mean ± SEM (n=3). *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001.

Techniques: Enzyme-linked Immunosorbent Assay

Review

brevilin a (MedChemExpress)

Structured Review

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1) Product Images from "Mechanistic prediction and validation of Brevilin A Therapeutic effects in Lung Cancer"

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High Performance Liquid Chromatography:

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