HY-N0064R Search Results


anwulignan  (MedChemExpress)
94
MedChemExpress anwulignan
Luteolin inhibits the NF-κB signaling pathway. (A) Western blotting of pro IL-1β, NLRP3, Casp-1 p45, ASC, and GAPDH in BMDMs treated with apigenin, esculetin, gomisin N, schisanhenol, schisandrin A, schisandrin B, <t>anwulignan,</t> schisantherin A, schisandrin B, specnuezhenide, schisandrin, luteolin, quinic acid, and curcumenol (40 μM) for 4 h and then stimulated with LPS (50 ng/ml) for 1 h. (B,C) ELISA of TNF-α (B) and IL-6 (C) in SN from samples described in A. (D) Western blotting of pro IL-1β, NLRP3, Casp-1 p45, ASC, and GAPDH in BMDMs treated with luteolin for 4 h and then stimulated with LPS (50 ng/ml) for 1 h. (E,F) ELISA of TNF-α (E) and IL-6 (F) in SN from samples described in D. GAPDH served as a loading control. Data are represented as the mean ± SD using biological samples.
Anwulignan, 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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Luteolin inhibits the NF-κB signaling pathway. (A) Western blotting of pro IL-1β, NLRP3, Casp-1 p45, ASC, and GAPDH in BMDMs treated with apigenin, esculetin, gomisin N, schisanhenol, schisandrin A, schisandrin B, anwulignan, schisantherin A, schisandrin B, specnuezhenide, schisandrin, luteolin, quinic acid, and curcumenol (40 μM) for 4 h and then stimulated with LPS (50 ng/ml) for 1 h. (B,C) ELISA of TNF-α (B) and IL-6 (C) in SN from samples described in A. (D) Western blotting of pro IL-1β, NLRP3, Casp-1 p45, ASC, and GAPDH in BMDMs treated with luteolin for 4 h and then stimulated with LPS (50 ng/ml) for 1 h. (E,F) ELISA of TNF-α (E) and IL-6 (F) in SN from samples described in D. GAPDH served as a loading control. Data are represented as the mean ± SD using biological samples.

Journal: Frontiers in Pharmacology

Article Title: An Integrative Pharmacology Based Analysis of Refined Liuweiwuling Against Liver Injury: A Novel Component Combination and Hepaprotective Mechanism

doi: 10.3389/fphar.2021.747010

Figure Lengend Snippet: Luteolin inhibits the NF-κB signaling pathway. (A) Western blotting of pro IL-1β, NLRP3, Casp-1 p45, ASC, and GAPDH in BMDMs treated with apigenin, esculetin, gomisin N, schisanhenol, schisandrin A, schisandrin B, anwulignan, schisantherin A, schisandrin B, specnuezhenide, schisandrin, luteolin, quinic acid, and curcumenol (40 μM) for 4 h and then stimulated with LPS (50 ng/ml) for 1 h. (B,C) ELISA of TNF-α (B) and IL-6 (C) in SN from samples described in A. (D) Western blotting of pro IL-1β, NLRP3, Casp-1 p45, ASC, and GAPDH in BMDMs treated with luteolin for 4 h and then stimulated with LPS (50 ng/ml) for 1 h. (E,F) ELISA of TNF-α (E) and IL-6 (F) in SN from samples described in D. GAPDH served as a loading control. Data are represented as the mean ± SD using biological samples.

Article Snippet: Apigenin, esculetin, gomisin N, schisanhenol, schisandrin A, schisandrin B, anwulignan, schisantherin A, schisantherin B, specnuezhenide, schisandrin, luteolin, quinic acid, curcumenol, and acetaminophen (APAP) were obtained from MCE (New Jersey, NJ, United States).

Techniques: Western Blot, Enzyme-linked Immunosorbent Assay, Control

Luteolin and esculetin suppress H 2 O 2 -induced apoptosis. (A) Apoptosis of L02 cells treated with apigenin, esculetin, gomisin N, schisanhenol, schisandrin A, schisandrin B, anwulignan, schisantherin A, schisantherin B, specnuezhenide, schisandrin, luteolin, quinic acid, and curcumenol (40 μM) and then exposed to APAP, as detected by flow cytometry. (B) The percentage of early apoptotic cells from samples described in A. (C) The percentage of total apoptotic cells from samples described in A. (D) Apoptosis of L02 cells treated with esculetin or luteolin (5, 10, and 20 μM) and then exposed to APAP, as detected by flow cytometry. (E–G) The percentage of early apoptotic cells (E) , late apoptotic cells (F) , and total apoptotic cells (G) treated with luteolin (5, 10, and 20 μM). (H–J) The percentage of early apoptotic cells (H) , late apoptotic cells (I) , and total apoptotic cells (J) treated with esculetin (5, 10, and 20 μM). Data are represented as the mean ± SD using biological samples. The significance of the differences was analyzed using unpaired Student’s t-test: *p < 0.05, **p < 0.01, ***p < 0.001 vs. the control, NS, not significant.

Journal: Frontiers in Pharmacology

Article Title: An Integrative Pharmacology Based Analysis of Refined Liuweiwuling Against Liver Injury: A Novel Component Combination and Hepaprotective Mechanism

doi: 10.3389/fphar.2021.747010

Figure Lengend Snippet: Luteolin and esculetin suppress H 2 O 2 -induced apoptosis. (A) Apoptosis of L02 cells treated with apigenin, esculetin, gomisin N, schisanhenol, schisandrin A, schisandrin B, anwulignan, schisantherin A, schisantherin B, specnuezhenide, schisandrin, luteolin, quinic acid, and curcumenol (40 μM) and then exposed to APAP, as detected by flow cytometry. (B) The percentage of early apoptotic cells from samples described in A. (C) The percentage of total apoptotic cells from samples described in A. (D) Apoptosis of L02 cells treated with esculetin or luteolin (5, 10, and 20 μM) and then exposed to APAP, as detected by flow cytometry. (E–G) The percentage of early apoptotic cells (E) , late apoptotic cells (F) , and total apoptotic cells (G) treated with luteolin (5, 10, and 20 μM). (H–J) The percentage of early apoptotic cells (H) , late apoptotic cells (I) , and total apoptotic cells (J) treated with esculetin (5, 10, and 20 μM). Data are represented as the mean ± SD using biological samples. The significance of the differences was analyzed using unpaired Student’s t-test: *p < 0.05, **p < 0.01, ***p < 0.001 vs. the control, NS, not significant.

Article Snippet: Apigenin, esculetin, gomisin N, schisanhenol, schisandrin A, schisandrin B, anwulignan, schisantherin A, schisantherin B, specnuezhenide, schisandrin, luteolin, quinic acid, curcumenol, and acetaminophen (APAP) were obtained from MCE (New Jersey, NJ, United States).

Techniques: Flow Cytometry, Control

Schisandrin A and schisandrin B inhibit the release of ROS. (A) HepaG2 cells were treated with apigenin, esculetin, gomisin N, schisanhenol, schisandrin A, schisandrin B, anwulignan, schisantherin A, schisantherin B, specnuezhenide, schisandrin, luteolin, quinic acid, and curcumenol (40 μM) before being stimulated with APAP. HepaG2 were loaded with MitoSOX red mitochondrial superoxide indicator (Ex/Em: 510/580 nm). After staining and washing, flow cytometry was conducted to test mtROS production. (B) Percentage of ROS-positive cells in HepaG2 cells from samples described in A. (C) The production of mtROS was detected by flow cytometry in HepaG2 cells treated with schisandrin A or schisandrin B (10, 20, and 40 μM). (D,E) Percentage of ROS-positive cells in HepaG2 cells pretreated with schisandrin A (D) or schisandrin B (E) (10, 20, and 40 μM) and then stimulated with APAP, followed by staining with MitoSox. Data are represented as the mean ± SD using biological samples. The significance of the differences was analyzed using unpaired Student’s t-test: *p < 0.05, **p < 0.01, ***p < 0.001 vs. the control, NS, not significant.

Journal: Frontiers in Pharmacology

Article Title: An Integrative Pharmacology Based Analysis of Refined Liuweiwuling Against Liver Injury: A Novel Component Combination and Hepaprotective Mechanism

doi: 10.3389/fphar.2021.747010

Figure Lengend Snippet: Schisandrin A and schisandrin B inhibit the release of ROS. (A) HepaG2 cells were treated with apigenin, esculetin, gomisin N, schisanhenol, schisandrin A, schisandrin B, anwulignan, schisantherin A, schisantherin B, specnuezhenide, schisandrin, luteolin, quinic acid, and curcumenol (40 μM) before being stimulated with APAP. HepaG2 were loaded with MitoSOX red mitochondrial superoxide indicator (Ex/Em: 510/580 nm). After staining and washing, flow cytometry was conducted to test mtROS production. (B) Percentage of ROS-positive cells in HepaG2 cells from samples described in A. (C) The production of mtROS was detected by flow cytometry in HepaG2 cells treated with schisandrin A or schisandrin B (10, 20, and 40 μM). (D,E) Percentage of ROS-positive cells in HepaG2 cells pretreated with schisandrin A (D) or schisandrin B (E) (10, 20, and 40 μM) and then stimulated with APAP, followed by staining with MitoSox. Data are represented as the mean ± SD using biological samples. The significance of the differences was analyzed using unpaired Student’s t-test: *p < 0.05, **p < 0.01, ***p < 0.001 vs. the control, NS, not significant.

Article Snippet: Apigenin, esculetin, gomisin N, schisanhenol, schisandrin A, schisandrin B, anwulignan, schisantherin A, schisantherin B, specnuezhenide, schisandrin, luteolin, quinic acid, curcumenol, and acetaminophen (APAP) were obtained from MCE (New Jersey, NJ, United States).

Techniques: Staining, Flow Cytometry, Control