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Showing papers on "Acacetin published in 2017"


Journal ArticleDOI
31 Aug 2017-PLOS ONE
TL;DR: It is suggested that acacetin augments the cytotoxicity of doxorubicin at lower concentrations in lung cancer cells, which leads to more retention in the cells by modulating drug trasporter and thus enhances its therapeutic potential.
Abstract: Background Anthracyclines are efficient and potent agents to treat broad range of cancers but cytotoxicity induced by them limits their use in therapeutics. Use of plant-derived agents help to prevent or delay the process of cancer progression and their combination increases the anti-cancer potential of mainstream compound. However, multidrug resistance is major cause of treatment failure in cancer patients. Purpose In this study, combination treatments of fisetin or acacetin with doxorubicin were explored for their potential synergistic effect on non-small-cell lung carcinoma (NSCLC) cells. Study design During this study, NSCLC model cell lines A549 and H1299 were used to determine the combinatorial effect of phytochemicals namly acacetin and fisetin with doxorubicin. Methods The effects of individual compounds and their combination on cell viability, clonogenic potential and cell cycle progression were studied. Efflux of doxorubicin was measured by spectrofluorophotometer, whereas accumulation inside the cells was analyzed by flow cytometry and confocal microscopy. Expression of MDR1 was checked by semi-quantitative PCR. Results The results showed that the cell viability of A549 and H1299 cells were significantly decreased in time- and dose-dependent manner, although A549 cells showed more sensitivity toward doxorubicin than H1299 cells. Mostly, combination of doxorubicin showed good synergy with acacetin in both the cell lines whereas, fisetin exerted synergistic effect only at 72 h of treatment in H1299 cells. Acacetin with doxorubicin caused G2/M arrest by downregulating CDK-cyclin complex in A549 cells. Acacetin-doxorubicin combination decreased the clonogenic potential of A549 and H1299 cells upto 82% and 59%, respectively, as compared to control. Acacetin also decreased efflux of doxorubicin by 59% after 30 mins of exposure to A549 cells and further increased accumulation of doxorubicin inside the cells upto 55% in 2 h. The modulatory effect of acacetin-doxorubicin combination on doxorubicin influx and efflux was mediated through downregulation of MDR1 treansporter in NSCLC cells. Conclusion These findings suggested that acacetin augments the cytotoxicity of doxorubicin at lower concentrations in lung cancer cells. Their combination leads to more retention of doxorubicin in the cells by modulating drug trasporter and thus enhances its therapeutic potential.

49 citations


Journal ArticleDOI
TL;DR: The data demonstrate that the metabolism of hydroxylated flavonoids by cytochrome P450 CYP1 enzymes, notably CYP 1A1 and CYB1B1, can enhance their antiproliferative activity in breast cancer cells.

42 citations


Journal ArticleDOI
TL;DR: The results suggest that acacetin is a potent therapeutic agent for PD progression and could inhibit 6-OHDA-induced neuronal cell death originating from ROS-mediated cascade apoptosis pathway.

41 citations


Journal ArticleDOI
TL;DR: It is demonstrated that acacetin inhibited adipogenesis in adipocytes and in obese mice, and reduced both body weight and visceral adipose tissue weight.
Abstract: Acacetin, a flavone that can be isolated from the Saussurea involucrata plant, has anti-tumor and anti-inflammatory properties that ameliorate airway hyperresponsiveness in asthmatic mice. This study investigated whether acacetin has anti-adipogenic effects in 3T3-L1 adipocytes and whether it regulates the inflammatory response in adipocytes and macrophages. It also investigated whether acacetin ameliorates lipid accumulation in high-fat diet- (HFD) induced obese mice. Differentiated 3T3-L1 cells were treated with acacetin. The glycerol levels in the culture medium were measured, and the expression of proteins and genes involved in adipogenesis and lipolysis were assayed by Western blot and real-time PCR, respectively. Inflammatory cytokine signaling pathway activity was assessed in macrophages that were treated with acacetin and cultured with differentiated medium from 3T3-L1 cells. Intraperitoneal injections of acacetin were administered to HFD-induced obese mice twice a week for 10 weeks. Acacetin significantly increased the levels of glycerol in the culture medium and significantly inhibited lipid accumulation in adipocytes. Acacetin reduced the expression of adipogenesis-related transcription factors, including the expression of the CCAAT/enhancer-binding protein; it also increased sirtuin 1 expression and AMPK phosphorylation in adipocytes. In macrophages cultured with differentiated media from 3T3-L1 adipocytes, acacetin reduced the levels of inflammatory mediators and the activity of the mitogen-activated protein kinase and NF-κB pathways. In obese mice, acacetin reduced both body weight and visceral adipose tissue weight. These results demonstrate that acacetin inhibited adipogenesis in adipocytes and in obese mice. Acacetin also reduced the inflammatory response of macrophages that were stimulated with differentiated media from 3T3-L1 cells.

39 citations


Journal ArticleDOI
TL;DR: In this article, five compounds were isolated from the leaves of Agastache rugosa and tested for monoamine oxidase (MAO) inhibitory activity: acacetin 7-O-(6-O-malonylglucoside) (AMG), Tilianin (a glucoside derivative of Acacetin), Amino acid (A.A. A.A., A.B., Cys172) and Amino acids (AA).

32 citations


Journal ArticleDOI
TL;DR: Collectively, acacetin improves mouse left ventricular function and attenuates cardiac remodeling by inhibiting of the MAPK and PI3K/Akt signaling pathway.

27 citations


Journal ArticleDOI
Pengran Cao1, Pingyao Xie1, Wang Xuebiao1, Jinmei Wang1, Jinfeng Wei1, Wenyi Kang1 
TL;DR: The results showed that the extract of A. rugosa possessed significant procoagulant activity, while its main components, acacetin and tilianin possessed significant anticoagULant activities.
Abstract: In the Chinese traditional medicine, plant of Agastache rugosa (Fisch. & C.A. Mey.) Kuntze (A. rugosa) has been used to treat nausea, vomiting and dispel damp. However, currently, few reports about the chemical constituents, especially the non-volatile components of A. rugosa are available. Through separation with various column chromatographies to elucidate the chemical constituents of A. rugosa, the biological activities of the major constituents were investigated. The extracts and main constituents of A. rugosa were evaluated for their anticoagulant effects by assaying the activated partial thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT) and fibrinogen (FIB) in vitro. Seven known compounds (namely compounds 1–7) were isolated from the aerial parts of A. rugosa. They were identified as methyl hexadecanoate (1), β-sitosterol (2), acacetin (3), ursolic acid (4), apigenin (5), protocatechuic acid (6) and tilianin (7), respectively. Compounds 1 and 6 were isolated from the genus Agastache for the first time, and compound 4 was obtained from the plants for the first time. The results showed that the extract of A. rugosa had a significant procoagulant activity by shortening the time of PT (P < 0.001) and increasing FIB content (P < 0.001), as compared with Vitamin K1. While its major constituents acacetin and tilianin exhibited significant anticoagulant activities by prolonging the times of PT, APTT, TT and reducing FIB content (P < 0.001), as compared with blank control group. The total extract of A. rugosa possessed significant procoagulant activity, while its main components, acacetin and tilianin possessed significant anticoagulant activities. Further investigation should be pursued to find out the bioactivity components responsible for the procoagulant action of the plant.

26 citations


Journal ArticleDOI
TL;DR: RARγ is reported as a negative regulator of p53 signaling and thus extended the oncogenic potential of RARγ to a new role in controlling the balance between AKT and p53.
Abstract: We recently demonstrated that retinoic acid receptor-γ (RARγ) is overexpressed and acts as a tumor promoter in hepatocellular carcinoma (HCC). The oncogenic activity of RARγ is mainly attributed to its physiological interaction with p85α regulatory subunit of PI3K leading to constitutive activation of AKT. Here we report RARγ as a negative regulator of p53 signaling and thus extend the oncogenic potential of RARγ to a new role in controlling the balance between AKT and p53. A natural flavonoid acacetin is then identified to be capable of modulating RARγ-dependent AKT-p53 network. It specifically binds to RARγ and inhibits all-trans retinoic acid (atRA) stimulation of RARγ transactivation. However, the anticancer action of acacetin is independent on its modulation of RARγ-driven transcriptional activity. Acacetin induces cancer cell apoptosis through antagonizing the non-genomic effect of RARγ on AKT and p53. When bound to RARγ, acacetin prevents RARγ from its activation of AKT followed by recovery of the normal p53 signaling. Given the implication of AKT-p53 dysregulation in most HCC, targeting the non-genomic signaling of RARγ that switches AKT-p53 from a pro-survival to a pro-apoptotic program in cancer cells should be a promising strategy for developing novel anti-HCC drugs.

21 citations


Journal ArticleDOI
TL;DR: The results from the present study provide further information about the flavonoids as taxonomic marker of the genus Chromolaena, and the chemotaxonomic significance of these compounds were also summarized.

20 citations


Journal ArticleDOI
TL;DR: The preliminary structure–activity relationship analysis suggests that the 3-O-glycosylation moiety in natural flavonoids was not essential for the antiproliferative activity on LOVO and U2-OS cells.
Abstract: Background: Limonium bicolor, a halophytic species, can grow in saline or saline-alkali soil, is well known as a traditional Chinese medicine. Recently it attracted much attention for its treatment for cancer. Objective: The present study was performed to evaluate this species from the phytochemical standpoint and the possible relationship between the antitumor activity and its natural products. Materials and methods: The chemical constituents from the flowers of L. bicolor were investigated through bioassay-guided fractionation and isolation. All the individual compounds were characterized by spectroscopic analysis and their potential antitumor activity was tested against three different human tumor cell lines by MTT assays. Results: The EtOAc extract was proven as the most potent fraction and further fractionation led to the isolation of 15 natural flavonoids, which were characterized as luteolin (1), acacetin (2), quercetin (3), isorhamnetin (4), kaempferol (5), eriodictyol (6), kaempferol-3-O-α-L-rhamnoside (7), kaempferol-3-O-β-D-glucoside (8), quercetin-3-O-α-L-rhamnoside (9), quercetin-3-O-β-D-glucoside (10), quercetin-3-O-β-D-galactoside (11), myricetin-3-O-α-L-rhamnoside (12), kaempferol-3-O-(6″-O-galloyl)-β-D-glucoside (13), hesperidin (14) and rutin (15). The biotesting results demonstrated that both compounds 1 and 3 showed good cytotoxicity against human colon cancer cells (LOVO). Compound 5 exhibited relative greater growth inhibition against both human breast cancer cells (MCF-7) and osteosarcoma cell lines (U2-OS) at the concentration of 100 μg/mL. Conclusion: On the basis of these findings, the flavonoids were deduced to be potentially responsible for the antitumor activity of L. bicolor. The preliminary structure–activity relationship analysis suggests that the 3-O-glycosylation moiety in natural flavonoids was not essential for the antiproliferative activity on LOVO and U2-OS cells. Abbreviation used: MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, EtOAc: Ethyl acetate; LOVO: human colon cancer; MCF-7: human breast, cancer; U2-OS: human osteosarcoma; 5-FU: 5-Fluorouracil; DMSO: dimethyl sulfoxide, NMR: nuclear magnetic resonance; HR-ESI-MS: high resolution electrospray ionization mass chromatography, HPLC: high performance liquid chromatography, EtOH: ethanol; n-BuOH: n-butanol; CC: column chromatography, TLC: thin layer chromatography; PBS: phosphate-buffered saline.

19 citations


Journal ArticleDOI
TL;DR: The novel information that acacetin remarkably inhibits SKCa channels, but not IKCa or BKCa channels is demonstrated, which suggests that blockade of SKCa by ac acetin likely contributes to its anti-AF property previously observed in experimental AF.
Abstract: The natural flavone acacetin inhibits several voltage-gated potassium currents in atrial myocytes, and has anti-atrial fibrillation (AF) effect in experimental AF models. The present study investigates whether acacetin inhibits the Ca2+-activated potassium (KCa) currents, including small conductance (SKCa1, SKCa2, and SKCa3), intermediate conductance (IKCa), and large-conductance (BKCa) channels stably expressed in HEK 293 cells. The effects of acacetin on these KCa channels were determined with a whole-cell patch voltage-clamp technique. The results showed that acacetin inhibited the three subtype SKCa channel currents in concentration-dependent manner with IC50 of 12.4 μM for SKCa1, 10.8 μM for SKCa2, and 11.6 μM for SKCa3. Site-directed mutagenesis of SKCa3 channels generated the mutants H490N, S512T, H521N, and A537V. Acacetin inhibited the mutants with IC50 of 118.5 μM for H490N, 275.2 μM for S512T, 15.3 μM for H521N, and 10.6 μM for A537V, suggesting that acacetin interacts with the P-loop helix of SKCa3 channel. However, acacetin at 3-10 μM did not decrease, but induced a slight increase of BKCa (+70 mV) by 8% at 30 μM. These results demonstrate the novel information that acacetin remarkably inhibits SKCa channels, but not IKCa or BKCa channels, which suggests that blockade of SKCa by acacetin likely contributes to its anti-AF property previously observed in experimental AF.

Journal ArticleDOI
TL;DR: It was found that the tyrosinase and melanogenesis inhibition was correlated with antioxidant activity of acacetin, the major biologically active substances in A. rugosa.
Abstract: SummaryBackground This work presents the first report that A. rugosa could have tyrosinase and melanogenesis inhibition and that its activities also be improved by fermentation with Lactobacillus rhamnosus and Lactobacillus paracasei. It was found that the tyrosinase and melanogenesis inhibition was correlated with antioxidant activity of acacetin, the major biologically active substances in A. rugosa. Aims we pursued an improvement in tyrosinase and melanogenesis inhibition of A. rugosa extract by fermentation process. Methods A. rugosa was extracted by lactic acid fermentation process; we measured antioxidant activities and tyrosinase and melanogenesis inhibition of A. rugosa extracts. Result In particular, reducing power of the extract from fermentation process (FE) was measured as 0.562 (O.D.), whereas reducing power of the extracts from 70% ethanol extraction (EE) was lower than the FE as 0.496 (O.D.). Polyphenols and flavonoids in the FE were higher than the EE: 69.3 mg/g vs. 60.5 mg/g, and 187 mg/g vs. 138 mg/g. The FE was estimated as 51.04% tyrosinase inhibition and 41.88% for the EE. Similarly, melanin inhibition in melanocyte B16F10 was observed as 66.60% vs. 42.23% for the FE and EE. The increase in tyrosinase and melanogenesis inhibition activity was confirmed by high elution of acacetin through fermentation process such as 289.97 mg/100 g vs. 198.04 mg/100 g in the FE and EE. Conclusion These results indicate that tyrosinase and melanogenesis inhibition activities of the extracts should be associated with antioxidant activity because acacetin is known to have strong antioxidant activity, which can also positively affect whitening activities.

Journal ArticleDOI
TL;DR: The results showed that acacetin-7-sulfate was the main metabolite mediated primarily by sulfotransferases (SULT) 1A1 and SULT1A1, BCRP, and MRP1 are responsible for acacet in- vivo exposure in vivo.
Abstract: Acacetin, an important component of acacia honey, exerts extensive therapeutic effects on many cancers. However, the sulfonation disposition of acacetin has rarely been reported. Therefore, this study aimed to investigate the sulfonation disposition of acacetin systematically. The results showed that acacetin-7-sulfate was the main metabolite mediated primarily by sulfotransferases (SULT) 1A1. Dog liver S9 presented the highest formation rate of acacetin-7-sulfate. Compared with that in wild-type Friend Virus B (FVB) mice, plasma exposure of acacetin-7-sulfate decreased significantly in multidrug resistance protein 1 knockout (Mrp1–/–) mice vut increased clearly in breast cancer resistance protein knockout (Bcrp–/–) mice. In Caco-2 monolayers, the efflux and clearance of acacetin-7-sulfate was reduced distinctly by the BCRP inhibitor Ko143 on the apical side and by the MRP1 inhibitor MK571 on the basolateral side. In conclusion, acacetin sulfonation was mediated mostly by SULT1A1. Acacetin-7-sulfate was f...

Journal ArticleDOI
TL;DR: In vivo feeding experiments indicated that PaF4′OMT could convert apigenin to acacetin efficiently in E. coli and approximately 88.8 µM (25.2 mg/L) of product was synthesized when 100 µM of apigen in was supplemented.
Abstract: Apigenin, a widely distributed flavone, exhibits excellent antioxidant, anti-inflammatory, and antitumor properties. In addition, the methylation of apigenin is generally considered to result in better absorption and greatly increased bioavailability. Here, four putative Class II methyltransferase genes were identified from the transcriptome sequences generated from the liverwort species Plagiochasma appendiculatum. Each was heterologously expressed as a His-fusion protein in Escherichia coli and their methylation activity against apigenin was tested. One of the four Class II OMT enzymes named 4′-O-methyltransferase (Pa4′OMT) was shown to react effectively with apigenin, catalyzing its conversion to acacetin. Besides the favorite substrate apigenin, the recombinant PaF4′OMT was shown to catalyze luteolin, naringenin, kaempferol, quercetin, genistein, scutellarein, and genkwanin to the corresponding 4′-methylation products. In vivo feeding experiments indicated that PaF4′OMT could convert apigenin to acacetin efficiently in E. coli and approximately 88.8 µM (25.2 mg/L) of product was synthesized when 100 µM of apigenin was supplemented. This is the first time that a Class II plant O-methyltransferase has been characterized in liverworts.

Journal ArticleDOI
TL;DR: The effect of various polyphenols, alkaloids, and terpenes-secondary metabolites produced by higher plants showing many beneficial properties for the human organism, on bacterial aminoacylation reaction showed that the most potent flavonoid inhibitors contain hydroxyl group at position 5 and 7 of A ring and OCH3 group at positions 4' of B ring.
Abstract: Tyrosyl-tRNA synthetases (TyrRSs) as essential enzymes for all living organisms are good candidates for therapeutic target in the prevention and therapy of microbial infection. We examined the effect of various polyphenols, alkaloids, and terpenes-secondary metabolites produced by higher plants showing many beneficial properties for the human organism, on bacterial aminoacylation reaction. The most potent inhibitors of Escherichia coli TyrRS are epigallocatechin gallate, acacetin, kaempferide, and chrysin, whereas the enzymes from Staphylococcus aureus and Pseudomonas aeruginosa are inhibited mainly by acacetin and chrysin. Most of them act as competitive inhibitors. Structure-activity relationship showed that the most potent flavonoid inhibitors contain hydroxyl group at position 5 and 7 of A ring and OCH3 group at position 4' of B ring.

Journal ArticleDOI
TL;DR: The coupling of glucuronidation and efflux transport was probably the primary reason for the low bioavailability of acacetin.
Abstract: To determine the mechanism responsible for acacetin glucuronide transport and the bioavailability of acacetin. Area under the curve (AUC), clearance (CL), half-life (T1/2) and other pharmacokinetic parameters were determined by the pharmacokinetic model. The excretion of acacetin glucuronides was evaluated by the mouse intestinal perfusion model and the Caco-2 cell model. In pharmacokinetic studies, the bioavailability of acacetin in FVB mice was 1.3%. Acacetin was mostly exposed as acacetin glucuronides in plasma. AUC of acacetin-7-glucuronide (Aca-7-Glu) was 2-fold and 6-fold higher in Bcrp1 (−/−) mice and Mrp2 (−/−) mice, respectively. AUC of acacetin-5-glucuronide (Aca-5-Glu) was 2-fold higher in Bcrp1 (−/−) mice. In mouse intestinal perfusion, the excretion of Aca-7-Glu was decreased by 1-fold and 2-fold in Bcrp1 (−/−) and Mrp2 (−/−) mice, respectively. In Caco-2 cells, the efflux rates of Aca-7-Glu and Aca-5-Glu were significantly decreased by breast cancer resistance protein (BCRP) inhibitor Ko143 and multidrug resistance protein 2 (MRP2) inhibitor LTC4. The use of these inhibitors markedly increased the intracellular acacetin glucuronide content. BCRP and MRP2 regulated the in vivo disposition of acacetin glucuronides. The coupling of glucuronidation and efflux transport was probably the primary reason for the low bioavailability of acacetin.


Journal ArticleDOI
TL;DR: It is demonstrated that acacetin induces not only apoptotic cell death via activation of Bak, loss of Δψ, and activation of the mitochondrial caspase cascade, but also cytoprotective autophagy resulting from suppression of the Akt-mTOR pathway.
Abstract: Exposure of Jurkat T cell clone (J/Neo cells) to acacetin (5,7-dihydroxy-4'-methoxyflavone), which is present in barnyard millet (Echinochloa esculenta (A. Braun)) grains, caused cytotoxicity, enhancement of apoptotic sub-G1 rate, Bak activation, loss of mitochondrial membrane potential (Δψ), activation of caspase-9 and caspase-3, degradation of poly(ADP-ribose) polymerase, and FITC-Annexin V-stainable phosphatidylserine exposure on the external surface of the cytoplasmic membrane without accompanying necrosis. These apoptotic responses were abrogated in Jurkat T cell clone (J/Bcl-xL) overexpressing Bcl-xL. Under the same conditions, cellular autophagic responses, including suppression of the Akt-mTOR pathway and p62/SQSTM1 down-regulation, were commonly detected in J/Neo and J/Bcl-xL cells; however, formation of acridine orange-stainable acidic vascular organelles, LC3-I/II conversion, and Beclin-1 phosphorylation (Ser-15) were detected only in J/Neo cells. Correspondingly, concomitant treatment with the autophagy inhibitor (3-methyladenine or LY294002) appeared to enhance acacetin-induced apoptotic responses, such as Bak activation, Δψ loss, activation of caspase-9 and caspase-3, and apoptotic sub-G1 accumulation. This indicated that acacetin could induce apoptosis and cytoprotective autophagy in Jurkat T cells simultaneously. Together, these results demonstrate that acacetin induces not only apoptotic cell death via activation of Bak, loss of Δψ, and activation of the mitochondrial caspase cascade, but also cytoprotective autophagy resulting from suppression of the Akt-mTOR pathway. Furthermore, pharmacologic inhibition of the autophagy pathway augments the activation of Bak and resultant mitochondrial damage-mediated apoptosis in Jurkat T cells.

Journal ArticleDOI
TL;DR: In this article, a liquid phase one-step synthesis of acacetin from ethyl 3-(4-methoxyphenyl)-3-oxopropionate and phloroglucinol using PEG 1000 as solvent was examined.
Abstract: In this work liquid phase one-step synthesis of acacetin from ethyl 3-(4-methoxyphenyl)-3-oxopropionate and phloroglucinol using PEG 1000 as solvent was examined. Heating of the reaction mixture was done with 915 MHz and 2.45 GHz microwaves at atmospheric pressure. The demethylation of the obtained acacetin using HBr at reflux led to the formation of apigenin. In view of a possible scale-up, the reaction conditions under 915 MHz microwaves were optimized to obtain high yields of acacetin. The energy required to convert phloroglucinol in acacetin was also estimated and used to calculate the total microwave power required for scaling up the process by a factor of 100. This method is an easier and cleaner synthesis for large scale preparation of flavones with good yields and purity.

Journal ArticleDOI
TL;DR: Fourteen compounds were isolated from the 80% ethanol extract of Caragana stenophylla root, by using a combination of various chromatographic approaches, including silica gel sephadex LH-20 column chromatography, and preparative HPLC, and revealed a new benzofuran derivative, named as mucodianin S.
Abstract: Fourteen compounds were isolated from the 80% ethanol extract of Caragana stenophylla root, by using a combination of various chromatographic approaches, including silica gel sephadex LH-20 column chromatography, and preparative HPLC. On the basis of their physical and chemical properties and spectroscopic data, their structures were elucidated as 2-(4-hydroxy-3-methoxy lphenyl)-3-methoxyl benzofuran-6-ol (1), mucodianin C (2), isopterofuran (3), formononetin (4), afromosin (5), calycosin (6), acacetin (7), 3-O-methylkaempferol (8), liquiritigenin (9), isoliquiritigenin (10), variabilin (11), resveratrol (12), zhebeiresinol (13), and 2, 3-dicarboxy-6, 7-dihydroxy-1-(3', 4'-dihydroxy)-phenyl-1, 2-dihydronaphthalen (14). Compound 1 is a new benzofuran derivative, named as mucodianin S; compounds 2, 3, 11, 13, 14 were isolated from the genus Caragana for the first time, and compounds 4-10 were firstly isolated from Caragana stenophylla. MTT assay was used to determine their cytotoxicity of the isolated compounds against human tumor cell lines, and 2 showed cytotoxicity against human hepato cellular cancer (HepG2) and human cervical (HeLa) lines, with IC₅₀ values of (16.18±0.95), (3.75±0.08) μmol•L ⁻¹, respectively.

Patent
29 Mar 2017
TL;DR: In this article, a dyeing method of acacetin on a dacron textile is described, which consists of the following steps that acacetins are dissolved in a carbon tetrachloride/phenol mixed solution, then a surface active agent sodium dodecyl benzene sulfonate is added, and a transparent solution is obtained under ultrasound images.
Abstract: The invention provides a dyeing method of acacetin on a dacron textile. The method comprises the following steps that acacetin is dissolved in a carbon tetrachloride/phenol mixed solution, then a surface active agent sodium dodecyl benzene sulfonate is added, and a transparent solution is obtained under ultrasounds; the dacron textile is put into the dyeing liquid, vibration heating is carried out till the temperature of 30 DEG C to 60 DEG C is achieved, and dyeing is carried out. According to the dyeing technology, the acacetin does not need to be modified, high temperature dyeing is not adopted, and the dyed textile is high in color fastness.

Patent
22 Sep 2017
TL;DR: The ointment provided by the invention has a good effect of promoting the healing of the postoperative wounds as discussed by the authors. But it is not suitable for the treatment of post-operative wounds.
Abstract: The invention provides ointment for promoting the healing of postoperative wounds. The ointment is prepared from active components and pharmaceutical auxiliary materials, wherein the active components comprise acacetin and albiflorin; preferably, the weight ratio of the acacetin to the albiflorin is (1 to 10) : 1. The ointment provided by the invention has a good effect of promoting the healing of the postoperative wounds.

Patent
Yang Ling, Wang Ping, Ge Guangbo, Dou Tongyi, Pan Cui 
24 May 2017
TL;DR: In this article, a method for preparing corresponding aglycone acacetin by enzymatic hydrolysis of buddleoside, and belongs to the field of bioengineering.
Abstract: The invention discloses a method for preparing corresponding aglycone acacetin by enzymatic hydrolysis of buddleoside, and belongs to the field of bioengineering. The method comprises crude enzyme fluid preparation, enzymatic hydrolysis and purification steps, specifically comprises the following steps: (1) preparation of a crude enzyme fluid: inoculating cellulosimicrobium cellulans into a liquid culture medium, performing culturing for 40h at 30 DEG C, performing 9,000g centrifugation for 10min, extracting supernatant, precipitating ammonium sulfate, collecting 20 to 40 percent of components, and performing re-dissolving with a buffer solution; (2) enzymatic hydrolysis: converting the buddleoside serving as a raw material with the dissolved crude enzyme fluid to hydrolyze beta-D-glucoside bonds of 7 loci to obtain the acacetin; and (3) preparation of the acacetin: after a reaction is completed, mixing the conversion solution and methanol in a double volume, heating to 60 DEG C, repeatedly extracting for 3 to 5 times, and collecting, cooling and crystalizing an extracting solution to obtain the acacetin. The method has the advantages of mild reaction condition, high specificity, high efficiency, low cost and the like, and the purity of the obtained acacetin is over 98 percent.