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3,6-Dihydroxyflavone

CAS# 108238-41-1

3,6-Dihydroxyflavone

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Chemical structure

3,6-Dihydroxyflavone

3D structure

Chemical Properties of 3,6-Dihydroxyflavone

Cas No. 108238-41-1 SDF Download SDF
PubChem ID 688659 Appearance Powder
Formula C15H10O4 M.Wt 254.2
Type of Compound Flavonoids Storage Desiccate at -20°C
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Chemical Name 3,6-dihydroxy-2-phenylchromen-4-one
SMILES C1=CC=C(C=C1)C2=C(C(=O)C3=C(O2)C=CC(=C3)O)O
Standard InChIKey XHLOLFKZCUCROE-UHFFFAOYSA-N
Standard InChI InChI=1S/C15H10O4/c16-10-6-7-12-11(8-10)13(17)14(18)15(19-12)9-4-2-1-3-5-9/h1-8,16,18H
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of 3,6-Dihydroxyflavone

Description3,6-Dihydroxyflavone is an anti-cancer agent, it induces apoptosis in leukemia HL-60 cell via reactive oxygen species-mediated p38 MAPK/JNK pathway. 3,6-Dihydroxyflavone is a potent agonist of the human peroxisome proliferator-activated receptor (hPPAR) with cytotoxic effects on human cervical cancer cells. 3,6-Dihydroxyflavone exhibits antibacterial activity against Gram-positive bacteria through inhibition of β-ketoacyl acyl carrier protein synthase III (KAS III).

3,6-Dihydroxyflavone Dilution Calculator

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Preparing Stock Solutions of 3,6-Dihydroxyflavone

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.9339 mL 19.6696 mL 39.3391 mL 78.6782 mL 98.3478 mL
5 mM 0.7868 mL 3.9339 mL 7.8678 mL 15.7356 mL 19.6696 mL
10 mM 0.3934 mL 1.967 mL 3.9339 mL 7.8678 mL 9.8348 mL
50 mM 0.0787 mL 0.3934 mL 0.7868 mL 1.5736 mL 1.967 mL
100 mM 0.0393 mL 0.1967 mL 0.3934 mL 0.7868 mL 0.9835 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on 3,6-Dihydroxyflavone

3,6-dihydroxyflavone suppresses the epithelial-mesenchymal transition, migration and invasion in endometrial stromal cells by inhibiting the Notch signaling pathway.[Pubmed:29949177]

Eur Rev Med Pharmacol Sci. 2018 Jun;22(12):4009-4017.

OBJECTIVE: Endometriosis is a common disease in women of reproductive age. Characteristics of endometriosis include invasion, metastasis, and recurrence, which are similar to those of malignant tumors. However, the etiology and pathogenesis of endometriosis are still not clear. This study aims to explore the mechanism of 3,6-Dihydroxyflavone (3,6-DHF) in the development of endometriosis. PATIENTS AND METHODS: Primary cultured ovarian ectopic endometrial stromal cells (OvESCs) were utilized as the in vitro model of endometriosis. OvESCs were treated with different concentrations of 3,6-DHF. The expressions of proteins related to epithelial-mesenchymal transition (EMT) and Notch signal pathway were detected by Western blot. The mRNA expressions of related genes were detected by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). The viability of treated cells was detected by transwell assay. The impact of 3,6-DHF on ectopic lesions was explored after the animal model of endometriosis was successfully established. RESULTS: With the increased concentration of 3,6-DHF in OvESCs, the protein and mRNA expressions of E-cadherin were gradually increased, while the protein and mRNA expressions of N-cadherin, Twist, Snail, and Slug were decreased. 3,6-DHF treatment inhibited the migration and invasion ability of OvESCs in a dose-dependent manner. In the endometriosis model of severe combined immunodeficient (SCID) mice, lesions in the 3,6-DHF treated group were significantly smaller than those of the control group. The same changes were found in the endometriosis model of Sprague Dawley (SD) rats. Protein expressions of Notch1, NICD, and Hes-1 in OvESCs were inhibited by 3,6-DHF in a dose-dependent manner. 3,6-DHF can inhibit the binding of NICD-CSL-MAML complex in OvESCs, thereby inhibiting the expressions of proteins related to Notch signaling pathway in vitro. CONCLUSIONS: 3,6-DHF can inhibit the development of EMT, migration, and invasion of endometrial stromal cells by inhibiting the Notch signaling pathway.

The high affinity of small-molecule antioxidants for hemoglobin.[Pubmed:29928975]

Free Radic Biol Med. 2018 Aug 20;124:260-274.

Hemoglobin has previously been shown to display ascorbate peroxidase and urate peroxidase activity, with measurable Michaelis-Menten parameters that reveal a particularly low Km for ascorbate as well as for urate - lower than the respective in vivo concentrations of these antioxidants in blood. Also, direct detection of a hemoglobin-ascorbate interaction was possible by monitoring the 1H-NMR spectrum of ascorbate in the presence of hemoglobin. The relative difference in structures between ascorbate and urate may raise the question as to exactly what the defining structural features would be, for a substrate that binds to hemoglobin with high affinity. Reported here are Michaelis-Menten parameters for hemoglobin acting as peroxidase against a number of other substrates of varying structures - gallate, caffeate, rutin, 3-hydroxyflavone, 3,6-Dihydroxyflavone, quercetin, epicatechin, luteolin - all with high affinities (some higher than those of physiologically-relevant redox partners of Hb - ascorbate and urate). Moreover, this high affinity appears general to animal hemoglobins. (1)H-NMR and (13)C-NMR spectra reveal a general pattern wherein small hydrophilic antioxidants appear to all have their signals affected, presumably due to binding to hemoglobin. Fluorescence and calorimetry measurements confirm these conclusions. Docking calculations confirm the existence of binding sites on hemoglobin and on myoglobin for ascorbate as well as for other antioxidants. Support is found for involvement of Tyr42 in binding of three out of the four substrates investigated in the case of hemoglobin (including ascorbate and urate, as blood-contained relevant substrates), but also for Tyr145 (with urate and caffeate) and Tyr35 (with gallate).

3,6-Dihydroxyflavone regulates microRNA-34a through DNA methylation.[Pubmed:28870206]

BMC Cancer. 2017 Sep 5;17(1):619.

BACKGROUND: Breast cancer is the common cancer in China. In previous study, we determined that 3,6-Dihydroxyflavone (3,6-DHF) increases miR-34a significantly in breast carcinogenesis, but the mechanism remains unclear. METHODS: We used qRT-PCR to analyze miR-34a and ten-eleven translocation (TET)1, TET2, TET3 levels in breast cancer cells. With a cellular breast carcinogenesis model and an experimental model of carcinogenesis in rats, TET1 levels were evaluated by western blot analysis and immunofluorescence. TET1 and 5hmC (5-hydroxymethylcytosine) levels were evaluated by immunofluorescence in nude mouse xenografts of MDA-MB-231 cells. Chromatin immunoprecipitation(ChIP) assayed for TET1 on the TET1 promoter, and dot blot analysis of DNA 5hmC was performed in MDA-MB-231 cells. We evaluated the mechanism of 3,6-DHF on the expression of tumor suppressor miR-34a by transfecting them with DNA methyltransferase (DNMT)1 plasmid and TET1 siRNA in breast cancer cells. Methylation-specific PCR detected methylation of the miR-34a promoter. RESULTS: First, we found that 3,6-DHF promotes the expression of TET1 during carcinogen-induced breast carcinogenesis in MCF10A cells and in rats. 3,6-DHF also increased TET1 and 5hmC levels in MDA-MB-231 cells. Further study indicated that TET1 siRNA and pcDNA3/Myc-DNMT1 inhibited the 3,6-DHF reactivation effect on expression of miR-34a in breast cancer cells. Methylation-specific PCR assays indicated that TET1 siRNA and pcDNA3/Myc-DNMT1 inhibit the effect of 3,6-DHF on the demethylation of the miR-34a promoter. CONCLUSIONS: Our study showed that 3,6-DHF effectively increases TET1 expression by inhibiting DNMT1 and DNA hypermethylation, and consequently up-regulates miR-34a in breast carcinogenesis.

3,6-dihydroxyflavone suppresses the epithelial-mesenchymal transition in breast cancer cells by inhibiting the Notch signaling pathway.[Pubmed:27345219]

Sci Rep. 2016 Jun 27;6:28858.

The epithelial to mesenchymal transition (EMT) is a critical developmental program in cancer stem cell (CSC) maintenance and in cancer metastasis. Here, our study found that 3,6-DHF could effectively inhibit EMT in BC cells in vitro and in vivo. 3,6-DHF effectively inhibits the formation and proliferation of BCSCs, and consequently reduces the tumor-initiating capacity of tumor cells in NOD/SCID mice. Optical in vivo imaging of cancer metastasis showed that 3,6-DHF administration suppresses the lung metastasis of BC cells in vivo. Further studies indicated that 3,6-DHF down-regulates Notch1, NICD, Hes-1 and c-Myc, consequently decreasing the formation of the functional transcriptional unit of NICD-CSL-MAML, causing Notch signaling inactivation in BC cells. Over-expression of Notch1 or inhibition of miR-34a significantly reduced the inhibitory effects of 3,6-DHF on EMT, CSCs, as well as cells migration and invasion in BC cells. These data indicated that 3,6-DHF effectively inhibits EMT and CSCs, as well as cells migration and invasion in BC cells, in which miR-34a-mediated Notch1 down-regulation plays a crucial role.

3,6-Dihydroxyflavone Suppresses Breast Carcinogenesis by Epigenetically Regulating miR-34a and miR-21.[Pubmed:25784176]

Cancer Prev Res (Phila). 2015 Jun;8(6):509-17.

Our previous study selected a promising chemopreventive agent 3,6-Dihydroxyflavone (3,6-DHF) and found that 3,6-DHF significantly upregulates miR-34a and downregulates miR-21 in breast carcinogenesis, yet the upstream and downstream events of the anticancer mechanism remain unclear. The present study showed that 3,6-DHF cotreatment effectively inhibits carcinogens-induced breast carcinogenic transformation in human breast epithelial MCF10A cells. The data revealed the significant downregulation of miR-34a and upregulation of miR-21 in breast carcinogenesis, which could be mitigated by 3,6-DHF treatment. Methylation-specific PCR detections showed that 3,6-DHF inhibits the hypermethylation of the miR-34a promoter. Further studies indicated that 3,6-DHF is an effective methyltransferase (DNMT)1 inhibitor, docking to the putative cytosine pocket of the protein, and thus decreases the DNMT activity in a dose-dependent manner. Moreover, the ChIP-qPCR analysis for histone modifications showed that 3,6-DHF treatment significantly lowers the H3K9-14ac on the miR-21 promoter. In addition, our study revealed that 3,6-DHF represses the PI3K/Akt/mTOR signaling pathway in breast carcinogenesis in vitro and in vivo. Inhibition of miR-34a or overexpression of miR-21 significantly reduced the effects of 3,6-DHF on Notch-1 and PTEN, and consequently weakened the suppression of 3,6-DHF on PI3K/Akt/mTOR. We concluded that 3,6-DHF upregulates miR-34a via inhibiting DNMT1 and hypermethylation, whereas downregulates miR-21 by modulating histone modification, and consequently suppresses the PI3K/Akt/mTOR signaling pathway in breast carcinogenesis.

3,6-diHydroxyflavone/bovine serum albumin interaction in cyclodextrin medium: absorption and emission monitoring.[Pubmed:25541401]

Spectrochim Acta A Mol Biomol Spectrosc. 2015 Mar 5;138:628-36.

Photophysical properties of a bioactive flavonol which can be used as a model for polyhydroxylated natural flavonols, 3,6-Dihydroxyflavone (3,6-diHF) in cyclodextrins (CDs)/bovine serum albumin (BSA) systems have been studied by absorption and fluorescence spectroscopy. The influence of CDs nature and of the different molar ratios BSA/CDs on the fluorescent characteristics of 3,6-diHF, and on the excited - state intramolecular proton transfer (ESIPT) process were studied. Quantitative information on the interaction between 3,6-diHF and BSA in CDs medium, were estimated. The influence of temperature (25-60 degrees C range) on the intrinsic fluorescence of BSA in 3,6-diHF/BSA/CDs systems, was investigated. The results are discussed with relevance to 3,6-diHF as a potential sensitive fluorescence probe in the systems of biological interest.

Cytotoxic activity of 3,6-dihydroxyflavone in human cervical cancer cells and its therapeutic effect on c-Jun N-terminal kinase inhibition.[Pubmed:25165860]

Molecules. 2014 Aug 27;19(9):13200-11.

Previously we have shown that 3,6-Dihydroxyflavone (3,6-DHF) is a potent agonist of the human peroxisome proliferator-activated receptor (hPPAR) with cytotoxic effects on human cervical cancer cells. To date, the mechanisms by which 3,6-DHF exerts its antitumor effects on cervical cells have not been clearly defined. Here, we demonstrated that 3,6-DHF exhibits a novel antitumor activity against HeLa cells with IC50 values of 25 muM and 9.8 muM after 24 h and 48 h, respectively. We also showed that the anticancer effects of 3,6-DHF are mediated via the toll-like receptor (TLR) 4/CD14, p38 mitogen-activated protein kinase (MAPK), Jun-N terminal kinase (JNK), extracellular-signaling regulated kinase (ERK), and cyclooxygenase (COX)-2 pathways in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. We found that 3,6-DHF showed a similar IC50 (113 nM) value to that of the JNK inhibitor, SP600125 (IC50 = 118 nM) in a JNK1 kinase assay. Binding studies revealed that 3,6-DHF had a strong binding affinity to JNK1 (1.996 x 105 M-1) and that the 6-OH and the carbonyl oxygen of the C ring of 3,6-DHF participated in hydrogen bonding interactions with the carbonyl oxygen and the amide proton of Met111, respectively. Therefore, 3,6-DHF may be a candidate inhibitor of JNKs, with potent anticancer effects.

Interference of selected flavonoid aglycons in platelet aggregation assays.[Pubmed:22868805]

Clin Chem Lab Med. 2012 Feb 28;50(8):1403-8.

BACKGROUND: Flavonoids are widely distributed across the plant kingdom and are therefore common ingredients in an everyday diet. Some flavonoids have a potential to affect platelet aggregation; most often antiaggregatory effects of flavonoids are observed. The objective of this research was to evaluate the in vitro effect of a selected set of flavonoids on platelet aggregation in whole blood. METHODS: The effect of five selected flavonoids (pinocembrin-7-methylether, epicatechin, hesperetin, 6-hydroxyflavone and 3,6-Dihydroxyflavone) on platelet aggregation was studied in the citrated whole blood samples collected from 75 healthy volunteers. A Multiplate((R)) impedance analyzer and five different aggregation inducers (ADP, arachidonic acid, collagen, ristocetin and TRAP-6) were utilized for the analysis of samples. RESULTS: Minimal antiaggregatory concentrations (MINaAC) of flavonoids in individual tests were reported in the following ranges: 0.12-1.91 muM; 15.26-244.14 muM; 15.26-122.07 muM; and 0.06-15.26 muM for ADP, collagen, TRAP-6 and ristocetin aggregation-inducers, respectively. When arachidonic acid was used for induction of platelet aggregation, a proaggregatory effect was observed for pinocembrin-7-methylether, epicatechin, hesperetin and 3,6-Dihydroxyflavone, while the expected antiaggregatory effect was observed only for 6-hydroxyflavone (MINaAC=7.63 muM). CONCLUSIONS: Flavonoids interfere with in vitro platelet aggregation assays exhibiting either anti- or proaggregatory effects in concentration ranges that can be achieved in circulation by dietary intake. Thus, dietary intake of flavonoids should be taken into account when interpreting the results of whole blood platelet aggregation.

MicroRNA-34a and microRNA-21 play roles in the chemopreventive effects of 3,6-dihydroxyflavone on 1-methyl-1-nitrosourea-induced breast carcinogenesis.[Pubmed:22616882]

Breast Cancer Res. 2012 May 22;14(3):R80.

INTRODUCTION: miRNAs are very important regulators in biological processes such as development, cellular differentiation, and carcinogenesis. Given the important role of miRNAs in tumorigenesis and development, it is worth investigating whether some miRNAs play roles in the anticancer mechanism of flavonoids. However, such a role has not yet been reported. We previously selected the promising anticancer agent 3,6-Dihydroxyflavone (3,6-DHF) in pharmacodynamic experiments, which may serve as a leading compound for developing more potent anticancer drugs or chemopreventive supplements. The present study aims to investigate the chemopreventive activities of 3,6-DHF against mammary carcinogenesis. METHODS: The experimental model of breast carcinogenesis was developed by intraperitoneal injection of 1-methyl-1-nitrosourea (MNU). The bioavailability of 3,6-DHF in rats was detected by HPLC. The expression of microRNA-34a (miR-34a) and microRNA-21 (miR-21) was evaluated by real-time quantitative RT-PCR. Cell apoptosis was analyzed by flow cytometry or terminal deoxynucleotidyl transferase dUTP nick end-labeling assay. The mitochondrial membrane potential was assayed using 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethyl-imidacarbocyanine iodide dye by confocal laser scanning microscopy. The level of cytochrome C in cytosol was evaluated by western blotting. RESULTS: Our study showed that oral administration of 3,6-DHF effectively suppressed MNU-induced breast carcinogenesis in rats, decreasing the cancer incidence by 35.7%. The detection of bioavailability indicated that the concentration of 3,6-DHF was 2.5 +/- 0.4 mug/ml in plasma of rats within 2 hours after administration, and was 21.7 +/- 3.8 mug/ml in urine within 24 hours. Oral administration of 3,6-DHF to BALB/c nude mice bearing breast cancer cell xenografts also significantly suppressed tumor growth in vivo. Furthermore, our study revealed that the global upregulation of miR-21 and downregulation of miR-34a in breast carcinogenesis could be reversed by 3,6-DHF, which significantly upregulated miR-34a expression and decreased miR-21 expression - inducing apoptosis of breast cancer cells in vitro and in vivo. Overexpression of miR-34a induced by plasmid transfection or inhibition of miR-21 by oligonucleotides markedly promoted the pro-apoptotic effect of 3,6-DHF. Inactivation of miR-34a or overproduction of miR-21 compromised the anticancer effects of 3,6-DHF. CONCLUSION: These findings indicate that 3,6-DHF is a potent natural chemopreventive agent, and that miR-34a and miR-21 play roles in MNU-induced breast carcinogenesis and the anticancer mechanism of flavonoids.

Evaluation of antiaggregatory activity of flavonoid aglycone series.[Pubmed:21745360]

Nutr J. 2011 Jul 11;10:73.

BACKGROUND: Among natural compounds, present in every day diet, flavonoids have shown beneficial effect in prevention of cardiovascular diseases that can be attributed, at least partially to the described antiaggregatory activity i.e. antiplatelet effects of flavonoids. Due to the ever increasing pharmacological interest in antiplatelet agents a systematic experimental evaluation of large flavonoid series is needed. METHODS: A set of thirty flavonoid aglycones has been selected for the evaluation. All measurements of aggregation were done under standardized and firmly controlled in vitro conditions. The whole blood samples, multiple platelet functional analyzer and adenosine diphosphate (ADP) as a weak agonist of aggregation were selected for this purpose. RESULTS: The results were expressed as minimal concentration of flavonoid that can significantly lower the platelet aggregation compared to the corresponding untreated sample (minimal antiaggregatory concentration--MINaAC). All analyzed flavonoids exhibited antiaggregatory activity MINaAC ranging from 0.119 muM to 122 muM, while the most potent representatives were 3,6-Dihydroxyflavone (0.119 muM) and syringetin (0.119 muM). CONCLUSIONS: Measurable antiplatelet activity established at submicromolar flavonoid concentrations suggests that even a dietary consumption of some flavonoids can make an impact on in vivo aggregation of platelets. These findings also point out a therapeutical potential of some flavonoids.

Quercetin-iron chelates are transported via glucose transporters.[Pubmed:21238582]

Free Radic Biol Med. 2011 Apr 15;50(8):934-44.

Flavonoids are well-known antioxidants and free radical scavengers. Their metal-binding activity suggests that they could be effective protective agents in pathological conditions caused by both extracellular and intracellular oxidative stress linked to metal overload. Quercetin is both a permeant ligand via glucose transport proteins (GLUTs) and a high-affinity inhibitor of GLUT-mediated glucose transport. Chelatable "free iron" at micromolar concentrations in body fluids is a catalyst of hydroxyl radical (OH(*)) production from hydrogen peroxide. A number of flavonoids, e.g., quercetin, luteolin, chrysin, and 3,6-Dihydroxyflavone, have been demonstrated to chelate intracellular iron and suppress OH(*) radical production in Madin Darby canine kidney cells. The most effective chelation comes from the flavonone B ring catechol found in both quercetin and luteolin. We show here that quercetin concentrations of <1muM can facilitate chelatable iron shuttling via GLUT1 in either direction across the cell membrane. These siderophoric effects are inhibited by raised quercetin concentrations (>1muM) or GLUT inhibitors, e.g., phloretin or cytochalasin B, and iron efflux is enhanced by impermeant extracellular iron chelators, either desferrioxamine or rutin. This iron shuttling property of quercetin might be usefully harnessed in chelotherapy of iron-overload conditions.

3,6-Dihydroxyflavone induces apoptosis in leukemia HL-60 cell via reactive oxygen species-mediated p38 MAPK/JNK pathway.[Pubmed:20840847]

Eur J Pharmacol. 2010 Dec 1;648(1-3):31-8.

We have previously selected a promising anti-cancer agent 3,6-Dihydroxyflavone by pharmacodynamic experiments. In the present study, we investigated its pro-apoptosis mechanisms in leukemia HL-60 cell. Our data revealed that 3,6-Dihydroxyflavone dose- and time-dependently decreases cell viability and induces apoptosis by activating caspase cascade, cleaving poly (ADP-ribose) polymerase (PARP). The anti-cancer effects of 3,6-Dihydroxyflavone are associated with the generation of reactive oxygen species, the altered glutathione-redox balance as significantly decreased glutathione (GSH) and its ratio to gluthatione disulfide (GSSG), and the accumulation of lipid peroxidation indicator malondialdehyde. Addition of antioxidant N-acetylcysteine (NAC) prevents the elevation of reactive oxygen species induced by 3,6-Dihydroxyflavone and partially suppresses the cytotoxic effects. Furthermore, 3,6-Dihydroxyflavone reduces cell membrane fluidity and induces the loss of mitochondrial membrane potential. 3,6-Dihydroxyflavone was also found to modulate the activities of mitogen-activated protein kinase (MAPK) family members, which includes increased protein kinase of 38 kDa (p38), c-Jun N-terminal kinase (JNK), and decreased extracellular signal-regulated kinase (ERK) activation. The effect of 3,6-Dihydroxyflavone on MAPKs pathway could be abrogated by co-treatment with NAC. Taking together, our data suggested that 3,6-Dihydroxyflavone increases intracellular oxidative stress and lipid peroxidation, thereby affecting the physical and functional properties of plasma membrane, as well as MAPKs signal pathway, which are likely to play a role in the 3,6-Dihydroxyflavone-induced HL-60 cell cytotoxicities.

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