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Acacetin

About: Acacetin is a research topic. Over the lifetime, 442 publications have been published within this topic receiving 10458 citations. The topic is also known as: 5,7-Dihydroxy-2-(4-methoxyphenyl)-4-benzopyrone & Linarigenin.


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Journal ArticleDOI
TL;DR: Results show that acacetin down regulates inflammatory iNOS and COX-2 gene expression in macrophages by inhibiting the activation of NF kappa B by interfering with the activation PI3K/Akt/IKK and MAPK, suggesting that ac acetin is a functionally novel agent capable of preventing inflammation-associated tumorigenesis.

142 citations

Journal ArticleDOI
Ye Yin1, Fangyuan Gong1, Xingxin Wu1, Yang Sun1, Yi-Hua Li1, Ting Chen1, Qiang Xu1 
TL;DR: The result suggests that cirsilineol, 6-methoxytricin and apigenin are the major active components in Artemisia vestita.

136 citations

Journal ArticleDOI
TL;DR: Propolis components such as artepillin C, caffeic acid phenethyl ester, galangin, kaempferol, and quercetin might represent a new class of dietary-derived antioxidative compounds with antiangiogenic activities that may have the potential to be developed into pharmaceutical drugs for the treatment of angiogenesis-dependent human diseases such as tumors.
Abstract: Propolis possesses various physiological activities. In this study, we examined the antiangiogenic and antioxidant activities of various components from propolis: acacetin, apigenin, artepillin C, caffeic acid phenethyl ester, chrysin, p-coumaric acid, galangin, kaempferol, pinocembrin, and quercetin. The effects of these components were tested on in vitro models of angiogenesis, tube formation and growth of human umbilical vein endothelial cells (HUVECs). Furthermore, these components were evaluated for their antioxidant activities by 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical-scavenging and ferric reducing/antioxidant power (FRAP) assays. Two propolis components, caffeic acid phenethyl ester, and quercetin, possessed strong inhibitory effects on tube formation and on endothelial cell proliferation and, coincidentally, showed strong antioxidant activity. Artepillin C, galangin, and kaempferol also possessed strong antiangiogenic and antioxidant activities to a slightly less degree. In contrast, acacetin, apigenin, and pinocembrin possessed a considerable degree of antiangiogenic activities, although they showed very low antioxidant activities. From these results, we propose that components from propolis such as artepillin C, caffeic acid phenethyl ester, galangin, kaempferol, and quercetin might represent a new class of dietary-derived antioxidative compounds with antiangiogenic activities. These propolis components may have the potential to be developed into pharmaceutical drugs for the treatment of angiogenesis-dependent human diseases such as tumors.

132 citations

Journal ArticleDOI
TL;DR: From the flowers ofChromolaena odorata four flavanones, isosakuranetin, persicogenin, 5,3′-dihydroxy-7,4′-dimethoxyflavanone, 4′-hydroxy-5,6,7,5′,6′-tetramethoxychalcone, and two flavones, acacetin and luteolin were isolated and identified.
Abstract: From the flowers ofChromolaena odorata (Eupatorium odoratum) four flavanones, isosakuranetin (5,7-dihydroxy-4′-methoxyflavanone) (1), persicogenin (5,3′-dihydroxy-7,4′-dimethoxyflavanone) (2), 5,6,7,4′-tetramethoxyflavanone (3) and 4′-hydroxy-5,6,7-trimethoxyflavanone (4), two chalcones, 2′-hydroxy-4,4′,5′,6′-tetramethoxychalcone (5) and 4,2′-dihydroxy-4′, 5′,6′-trimethoxychalcone (6), and two flavones, acacetin (5,7-dihydroxy-4′-methoxyflavone) (7) and luteolin (5,7,3′,4′-tetrahydroxyflavone) (8) were isolated and identified. Compound 1 exhibited moderate antimycobacterial activity againstMycobacterium tuberculosis with the MIC value of 174.8 μM, whereas compounds4,7, and8 exhibited weak activity with the MIC values of 606.0, 704.2 and 699.3 μM respectively. Compound7 showed moderate cytotoxicity against human small cell lung cancer (NCI-H187) cells with the MIC value of 24.6 μM, whereas compound8 exhibited moderate toxicity against NCI-H187 cells and week toxicity against human breast cancer (BC) cells with the MIC values of 19.2 and 38.4 μM respectively.

127 citations

Journal ArticleDOI
TL;DR: The induction of cell-cycle arrest by five of seven tested apigenin analogs and the additive induction by the combination of flavonoids at low doses suggest that apigen in-related flavonoid may cooperatively protect against colorectal cancer through conjoint blocking of cell -cycle progression.
Abstract: Apigenin has been previously shown to induce G2/M cell-cycle arrest in human colon cancer cell lines. The present study assessed the individual and interactive influence of seven apigenin analogs on cell cycle, cell number, and cell viability in human SW480 and Caco-2 colonic carcinoma cells. Cellular concentration of selected apigenin analogs was further assessed by high-performance liquid chromatography to assess cellular availability. The apigenin analogs studied were acacetin, chrysin, kampherol, luteolin, myricetin, naringenin, and quercetin. DNA flow cytometric analysis indicated that treatment with either chrysin or acacetin at 0 to 80 microM for 48 h resulted in cell-cycle arrest at the G2/M phase in a dose-dependent manner in the SW480 cells but not in the Caco-2 cells. The percentage of SW480 cells at G2/M also increased when cells were treated with kampherol, luteolin, or quercetin between 5 and 30 microM, but the percentage of cells in G2/M decreased at doses greater than 40 microM. Cell number was significantly decreased in a time- and dose-dependent manner following the treatments with each analog except for naringenin and myricetin. The interactive effects of these analogs with apigenin were further assessed by combining each analog at doses from 0 to 80 microM with apigenin at 20 microM, a dose at which apigenin was found to double the proportion of SW480 cells in G2/M. When either acacetin, chrysin, luteolin, kampherol, or quercetin at doses between 5 and 30 microM were combined with apigenin at 20 microM, there was an increase of 22% in the proportion of G2/M cells over that observed with 20 microM apigenin alone (P < 0.05). At doses higher than 40 microM, however, the interaction became antagonistic, and the proportion of cells in G2/M decreased below that observed with apigenin alone. Cell viability, as assessed by Trypan blue exclusion assay, significantly decreased by treatments with high doses of each agent or each agent combined with apigenin. Cellular concentration of apigenin, chrysin, or naringenin in SW480 cells significantly increased at doses of 40 microM or greater, but it was not correlated with their impact on G2/M cell-cycle arrest. The induction of cell-cycle arrest by five of seven tested apigenin analogs and the additive induction by the combination of flavonoids at low doses suggest that apigenin-related flavonoids may cooperatively protect against colorectal cancer through conjoint blocking of cell-cycle progression.

127 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202320
202252
202127
202031
201923
201818