Wogonin

CAS# 632-85-9

Wogonin

Catalog No. BCN4171----Order now to get a substantial discount!

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Quality Control of Wogonin

Number of papers citing our products

Chemical structure

Wogonin

3D structure

Chemical Properties of Wogonin

Cas No. 632-85-9 SDF Download SDF
PubChem ID 5281703 Appearance Yellow powder
Formula C16H12O5 M.Wt 284.3
Type of Compound Flavonoids Storage Desiccate at -20°C
Synonyms 5,7-Dihydroxy 8-methoxyflavone
Solubility ≥56.33mg/mL in DMSO
Chemical Name 5,7-dihydroxy-8-methoxy-2-phenylchromen-4-one
SMILES COC1=C(C=C(C2=C1OC(=CC2=O)C3=CC=CC=C3)O)O
Standard InChIKey XLTFNNCXVBYBSX-UHFFFAOYSA-N
Standard InChI InChI=1S/C16H12O5/c1-20-15-12(19)7-10(17)14-11(18)8-13(21-16(14)15)9-5-3-2-4-6-9/h2-8,17,19H,1H3
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.

Source of Wogonin

The root of Scutellaria baicalensis Georgi

Biological Activity of Wogonin

DescriptionWogonin is an inhibitor of CDK9, which has anti-inflammatory and anti-tumor activities, it could be developed into an efficient natural sensitizer for resistant human myelogenous leukemia. It has a wide spectrum of targets including PGE2, NO, Nrf2, Src, MEK1/2, ERK1/2, NFκB,MLCK, MLC.
TargetsCaspase | Nrf2 | PGE | NO | Src | MEK | ERK | NF-kB | COX | VEGFR | TLR | DNA-PK | PI3K | Akt | IFN-γ | p65 | p38MAPK | JNK | MLCK | MLC | CDK9
In vitro

Wogonin induces eosinophil apoptosis and attenuates allergic airway inflammation.[Pubmed: 25629436]

Am J Respir Crit Care Med. 2015 Mar 15;191(6):626-36.

Eosinophils are key effector cells in allergic diseases, including allergic rhinitis, eczema, and asthma. Their tissue presence is regulated by both recruitment and increased longevity at inflamed sites. To investigate the ability of the flavone Wogonin to induce eosinophil apoptosis in vitro and attenuate eosinophil-dominant allergic inflammation in vivo in mice.
METHODS AND RESULTS:
Human and mouse eosinophil apoptosis in response to Wogonin was investigated by cellular morphology, flow cytometry, mitochondrial membrane permeability, and pharmacological caspase inhibition. Allergic lung inflammation was modeled in mice sensitized and challenged with ovalbumin. Bronchoalveolar lavage (BAL) and lung tissue were examined for inflammation, mucus production, and inflammatory mediator production. Airway hyperresponsiveness to aerosolized methacholine was measured. Wogonin induced time- and concentration-dependent human and mouse eosinophil apoptosis in vitro. Wogonin-induced eosinophil apoptosis occurred with activation of caspase-3 and was inhibited by pharmacological caspase inhibition. Wogonin administration attenuated allergic airway inflammation in vivo with reductions in BAL and interstitial eosinophil numbers, increased eosinophil apoptosis, reduced airway mucus production, and attenuated airway hyperresponsiveness. This Wogonin-induced reduction in allergic airway inflammation was prevented by concurrent caspase inhibition in vivo.
CONCLUSIONS:
Wogonin induces eosinophil apoptosis and attenuates allergic airway inflammation, suggesting that it has therapeutic potential for the treatment of allergic inflammation in humans.

Wogonin attenuates endotoxin-induced prostaglandin E2 and nitric oxide production via Src-ERK1/2-NFκB pathway in BV-2 microglial cells.[Pubmed: 23362215]

Environ Toxicol. 2014 Oct;29(10):1162-70.

Microglia are the major component of intrinsic brain immune system in neuroinflammation. Although Wogonin expresses anti-inflammatory function in microglia, little is known about the molecular mechanisms of the protective effect of Wogonin against microglia activation. The aim of this study was to evaluate how Wogonin exerts its anti-inflammatory function in BV2 microglial cells after LPS/INFγ administration.
METHODS AND RESULTS:
Wogonin not only inhibited LPS/ INFγ-induced PGE2 and NO production without affecting cell viability but also exhibited parallel inhibition on LPS/INFγ-induced expression of iNOS and COX-2 in the same concentration range. While LPS/INFγ-induced expression of P-p65 and P-IκB was inhibited by Wogonin-only weak inhibition on P-p38 and P-JNK were observed, whereas it significantly attenuated the P-ERK1/2 and its upstream activators P-MEK1/2 and P-Src in a parallel concentration-dependent manner.
CONCLUSIONS:
These results indicated that the blockade of PGE2 and NO production by Wogonin in LPS/INFγ-stimulated BV2 cells is attributed mainly to interference in the Src-MEK1/2-ERK1/2-NFκB-signaling pathway.

Protocol of Wogonin

Kinase Assay

Wogonin inhibits LPS-induced tumor angiogenesis via suppressing PI3K/Akt/NF-κB signaling.[Pubmed: 24858369]

Wogonin inhibits LPS-induced vascular permeability via suppressing MLCK/MLC pathway.[Pubmed: 25956732]

Vascul Pharmacol. 2015 May 5.

Wogonin, a naturally occurring monoflavonoid extracted from the root of Scutellaria baicalensis Georgi, has been shown to have anti-inflammatory and anti-tumor activities and inhibits oxidant stress-induced vascular permeability. However, the influence of Wogonin on vascular hyperpermeability induced by overabounded inflammatory factors often appears in inflammatory diseases and tumor is not well known. In this study, we evaluate the effects of Wogonin on LPS induced vascular permeability in human umbilical vein endothelial cells (HUVECs) and investigate the underlying mechanisms.
METHODS AND RESULTS:
We find that Wogonin suppresses the LPS-stimulated hyperactivity and cytoskeleton remodeling of HUVECs, promotes the expression of junctional proteins including VE-Cadherin, Claudin-5 and ZO-1, as well as inhibits the invasion of MDA-MB-231 across EC monolayer. Miles vascular permeability assay proves that Wogonin can restrain the extravasated Evans in vivo. The mechanism studies reveal that the expressions of TLR4, p-PLC, p-MLCK and p-MLC are decreased by Wogonin without changing the total steady state protein levels of PLC, MLCK and MLC. Moreover, Wogonin can also inhibit KCl-activated MLCK/MLC pathway, and further affect vascular permeability. Significantly, compared with wortmannin, the inhibitor of MLCK/MLC pathway, Wogonin exhibits similar inhibition effects on the expression of p-MLCK, p-MLC and LPS-induced vascular hyperpermeability.
CONCLUSIONS:
Taken together, Wogonin can inhibit LPS-induced vascular permeability by suppressing the MLCK/MLC pathway, suggesting a therapeutic potential for the diseases associated with the development of both inflammatory and tumor.

Eur J Pharmacol. 2014 Aug 15;737:57-69.

Wogonin has been shown to have anti-angiogenesis and anti-tumor effects. However, whether Wogonin inhibits LPS-induced tumor angiogenesis is not well known. In this study, we investigated the effect of Wogonin on inhibiting LPS-induced tumor angiogenesis and further probed the underlying mechanisms.
METHODS AND RESULTS:
ELISA results revealed that Wogonin could suppress LPS-induced VEGF secretion from tumor cells. Transwell assay, tube formation assay, rat aortic ring assay and CAM model were used to evaluate the effect of Wogonin on angiogenesis induced by MCF-7 cell (treated with LPS) in vitro and in vivo. The inhibitory effect of Wogonin on angiogenesis in LPS-treated MCF-7 cells was then confirmed by the above in vitro and in vivo assays. The study of the molecular mechanism showed that Wogonin could suppress PI3K/Akt signaling activation. Moreover, Wogonin inhibited nuclear translocation of NF-κB and its binding to DNA. The result of real-time PCR and luciferase reporter assay suggested that VEGF expression was down-regulated by Wogonin primarily at the transcriptional level. IGF-1 and p65 expression plasmid were used to activate PI3K/Akt and NF-κB pathways, and to observe the effect of Wogonin on the simualtion of PI3K/Akt/NF-κB signaling.
CONCLUSIONS:
Taken together, the result suggested that Wogonin was a potent inhibitor of tumor angiogenesis and provided a new insight into the mechanisms of Wogonin against cancer.

Cell Research

Wogonin reverses multi-drug resistance of human myelogenous leukemia K562/A02 cells via downregulation of MRP1 expression by inhibiting Nrf2/ARE signaling pathway.[Pubmed: 25264278]

Biochem Pharmacol. 2014 Nov 15;92(2):220-34.

Constitutive NF-E2-related factor 2 (Nrf2) activation has been recently reported to play a pivotal role in enhancing cell survival and resistance to anticancer drugs in many tumors. Previously, much effort has been devoted to the investigation of blocking Nrf2 function in cultured cells and cancer tissues, but few researches have been undertaken to evaluate the precise mechanism of flavonoids-induced sensitivity by inhibiting Nrf2. In this study, we investigated the reversal effect of Wogonin, a flavonoid isolated from the root of Scutellaria baicalensis Georgi, in resistant human myelogenous leukemia.
METHODS AND RESULTS:
Data indicated that Wogonin had strong reversal potency by inhibiting functional activity and expression of MRP1 at both protein and mRNA in adriamycin (ADR)-induced resistant human myelogenous leukemia K562/A02 cells. Consequently, the inhibition of MRP1 by Wogonin was dependent on Nrf2 through the decreased binding ability of Nrf2 to antioxidant response element (ARE). Further research revealed Wogonin modulated Nrf2 through the reduction of Nrf2mRNA at transcriptional processes rather than RNA degradation, which is regulated by the PI3K/Akt pathway. Moreover, DNA-PKcs was found to be involved in the Wogonin-induced downregulation of Nrf2 mRNA at transcriptional levels.
CONCLUSIONS:
In summary, these results clearly demonstrated the effectiveness of using Wogonin via inhibiting Nrf2 to combat chemoresistance and suggested that Wogonin can be developed into an efficient natural sensitizer for resistant human myelogenous leukemia.

Wogonin Dilution Calculator

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Preparing Stock Solutions of Wogonin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.5174 mL 17.5871 mL 35.1741 mL 70.3482 mL 87.9353 mL
5 mM 0.7035 mL 3.5174 mL 7.0348 mL 14.0696 mL 17.5871 mL
10 mM 0.3517 mL 1.7587 mL 3.5174 mL 7.0348 mL 8.7935 mL
50 mM 0.0703 mL 0.3517 mL 0.7035 mL 1.407 mL 1.7587 mL
100 mM 0.0352 mL 0.1759 mL 0.3517 mL 0.7035 mL 0.8794 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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Background on Wogonin

Wogonin is a naturally occurring mono-flavonoid, can inhibit the activity of CDK8 and Wnt, and exhibits anti-inflammatory and anti-tumor effects.

In Vitro:Wogonin (0-200 μM) exhibits a dose- and time- dependent reduces in cell viability of caco-2, SW1116 and HCT116 cells. Wogonin (10-40 μM) induces G1 phase arrest in HCT-116 cells. Wogonin also supresses Wnt signaling pathway in HCT116 cells. Wogonin interfers in the activity of transcription factor TCF/Lef family. Moreover, Wogonin inhibits β-catenin-mediated transcription through suppressing the activity of CDK8[1]. Wogonin shows cytotoxic and antiproliferative effects on HeLa cells. Wogonin (90 µM) induces cell cycle arrest at G0-G1 phase, and suppresses the levels of cyclin D1 and Cdk4 markedly in HeLa cells[2]. Wogonin (1.25, 2.5, 5, 10, 20 μg/ml) suppresses EtOH-induced inflammatory response in RAW264.7 cells[3].

In Vivo:Wogonin (30, 60 mg/kg) reduces tumor growth of HCT116 cells in a xenograft model[1]. Wogonin (25, 50, 100 mg/kg) protects against liver injury and pathological characteristics of ALD in mice. Wogonin activates PPAR-γ expression in mice with ALD and EtOH induced RAW264.7 cells[3].

References:
[1]. He L, et al. Wogonin induced G1 cell cycle arrest by regulating Wnt/β-catenin signaling pathway and inactivating CDK8 in human colorectal cancer carcinoma cells. Toxicology. 2013 Oct 4;312:36-47. [2]. Yang L, et al. Wogonin induces G1 phase arrest through inhibiting Cdk4 and cyclin D1 concomitant with an elevation in p21Cip1 in human cervical carcinoma HeLa cells. Biochem Cell Biol. 2009 Dec;87(6):933-42. [3]. Li HD, et al. Wogonin attenuates inflammation by activating PPAR-γ in alcoholic liver disease. Int Immunopharmacol. 2017 Sep;50:95-106.

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References on Wogonin

Wogonin attenuates endotoxin-induced prostaglandin E2 and nitric oxide production via Src-ERK1/2-NFkappaB pathway in BV-2 microglial cells.[Pubmed:23362215]

Environ Toxicol. 2014 Oct;29(10):1162-70.

Microglia are the major component of intrinsic brain immune system in neuroinflammation. Although Wogonin expresses anti-inflammatory function in microglia, little is known about the molecular mechanisms of the protective effect of Wogonin against microglia activation. The aim of this study was to evaluate how Wogonin exerts its anti-inflammatory function in BV2 microglial cells after LPS/INFgamma administration. Wogonin not only inhibited LPS/ INFgamma-induced PGE2 and NO production without affecting cell viability but also exhibited parallel inhibition on LPS/INFgamma-induced expression of iNOS and COX-2 in the same concentration range. While LPS/INFgamma-induced expression of P-p65 and P-IkappaB was inhibited by Wogonin-only weak inhibition on P-p38 and P-JNK were observed, whereas it significantly attenuated the P-ERK1/2 and its upstream activators P-MEK1/2 and P-Src in a parallel concentration-dependent manner. These results indicated that the blockade of PGE2 and NO production by Wogonin in LPS/INFgamma-stimulated BV2 cells is attributed mainly to interference in the Src-MEK1/2-ERK1/2-NFkappaB-signaling pathway.

Wogonin induces eosinophil apoptosis and attenuates allergic airway inflammation.[Pubmed:25629436]

Am J Respir Crit Care Med. 2015 Mar 15;191(6):626-36.

RATIONALE: Eosinophils are key effector cells in allergic diseases, including allergic rhinitis, eczema, and asthma. Their tissue presence is regulated by both recruitment and increased longevity at inflamed sites. OBJECTIVES: To investigate the ability of the flavone Wogonin to induce eosinophil apoptosis in vitro and attenuate eosinophil-dominant allergic inflammation in vivo in mice. METHODS: Human and mouse eosinophil apoptosis in response to Wogonin was investigated by cellular morphology, flow cytometry, mitochondrial membrane permeability, and pharmacological caspase inhibition. Allergic lung inflammation was modeled in mice sensitized and challenged with ovalbumin. Bronchoalveolar lavage (BAL) and lung tissue were examined for inflammation, mucus production, and inflammatory mediator production. Airway hyperresponsiveness to aerosolized methacholine was measured. MEASUREMENTS AND MAIN RESULTS: Wogonin induced time- and concentration-dependent human and mouse eosinophil apoptosis in vitro. Wogonin-induced eosinophil apoptosis occurred with activation of caspase-3 and was inhibited by pharmacological caspase inhibition. Wogonin administration attenuated allergic airway inflammation in vivo with reductions in BAL and interstitial eosinophil numbers, increased eosinophil apoptosis, reduced airway mucus production, and attenuated airway hyperresponsiveness. This Wogonin-induced reduction in allergic airway inflammation was prevented by concurrent caspase inhibition in vivo. CONCLUSIONS: Wogonin induces eosinophil apoptosis and attenuates allergic airway inflammation, suggesting that it has therapeutic potential for the treatment of allergic inflammation in humans.

Wogonin inhibits LPS-induced tumor angiogenesis via suppressing PI3K/Akt/NF-kappaB signaling.[Pubmed:24858369]

Eur J Pharmacol. 2014 Aug 15;737:57-69.

Wogonin has been shown to have anti-angiogenesis and anti-tumor effects. However, whether Wogonin inhibits LPS-induced tumor angiogenesis is not well known. In this study, we investigated the effect of Wogonin on inhibiting LPS-induced tumor angiogenesis and further probed the underlying mechanisms. ELISA results revealed that Wogonin could suppress LPS-induced VEGF secretion from tumor cells. Transwell assay, tube formation assay, rat aortic ring assay and CAM model were used to evaluate the effect of Wogonin on angiogenesis induced by MCF-7 cell (treated with LPS) in vitro and in vivo. The inhibitory effect of Wogonin on angiogenesis in LPS-treated MCF-7 cells was then confirmed by the above in vitro and in vivo assays. The study of the molecular mechanism showed that Wogonin could suppress PI3K/Akt signaling activation. Moreover, Wogonin inhibited nuclear translocation of NF-kappaB and its binding to DNA. The result of real-time PCR and luciferase reporter assay suggested that VEGF expression was down-regulated by Wogonin primarily at the transcriptional level. IGF-1 and p65 expression plasmid were used to activate PI3K/Akt and NF-kappaB pathways, and to observe the effect of Wogonin on the simualtion of PI3K/Akt/NF-kappaB signaling. Taken together, the result suggested that Wogonin was a potent inhibitor of tumor angiogenesis and provided a new insight into the mechanisms of Wogonin against cancer.

Wogonin reverses multi-drug resistance of human myelogenous leukemia K562/A02 cells via downregulation of MRP1 expression by inhibiting Nrf2/ARE signaling pathway.[Pubmed:25264278]

Biochem Pharmacol. 2014 Nov 15;92(2):220-34.

Constitutive NF-E2-related factor 2 (Nrf2) activation has been recently reported to play a pivotal role in enhancing cell survival and resistance to anticancer drugs in many tumors. Previously, much effort has been devoted to the investigation of blocking Nrf2 function in cultured cells and cancer tissues, but few researches have been undertaken to evaluate the precise mechanism of flavonoids-induced sensitivity by inhibiting Nrf2. In this study, we investigated the reversal effect of Wogonin, a flavonoid isolated from the root of Scutellaria baicalensis Georgi, in resistant human myelogenous leukemia. Data indicated that Wogonin had strong reversal potency by inhibiting functional activity and expression of MRP1 at both protein and mRNA in adriamycin (ADR)-induced resistant human myelogenous leukemia K562/A02 cells. Consequently, the inhibition of MRP1 by Wogonin was dependent on Nrf2 through the decreased binding ability of Nrf2 to antioxidant response element (ARE). Further research revealed Wogonin modulated Nrf2 through the reduction of Nrf2mRNA at transcriptional processes rather than RNA degradation, which is regulated by the PI3K/Akt pathway. Moreover, DNA-PKcs was found to be involved in the Wogonin-induced downregulation of Nrf2 mRNA at transcriptional levels. In summary, these results clearly demonstrated the effectiveness of using Wogonin via inhibiting Nrf2 to combat chemoresistance and suggested that Wogonin can be developed into an efficient natural sensitizer for resistant human myelogenous leukemia.

Wogonin inhibits LPS-induced vascular permeability via suppressing MLCK/MLC pathway.[Pubmed:25956732]

Vascul Pharmacol. 2015 Sep;72:43-52.

Wogonin, a naturally occurring monoflavonoid extracted from the root of Scutellaria baicalensis Georgi, has been shown to have anti-inflammatory and anti-tumor activities and inhibits oxidant stress-induced vascular permeability. However, the influence of Wogonin on vascular hyperpermeability induced by overabounded inflammatory factors often appears in inflammatory diseases and tumor is not well known. In this study, we evaluate the effects of Wogonin on LPS induced vascular permeability in human umbilical vein endothelial cells (HUVECs) and investigate the underlying mechanisms. We find that Wogonin suppresses the LPS-stimulated hyperactivity and cytoskeleton remodeling of HUVECs, promotes the expression of junctional proteins including VE-Cadherin, Claudin-5 and ZO-1, as well as inhibits the invasion of MDA-MB-231 across EC monolayer. Miles vascular permeability assay proves that Wogonin can restrain the extravasated Evans in vivo. The mechanism studies reveal that the expressions of TLR4, p-PLC, p-MLCK and p-MLC are decreased by Wogonin without changing the total steady state protein levels of PLC, MLCK and MLC. Moreover, Wogonin can also inhibit KCl-activated MLCK/MLC pathway, and further affect vascular permeability. Significantly, compared with wortmannin, the inhibitor of MLCK/MLC pathway, Wogonin exhibits similar inhibition effects on the expression of p-MLCK, p-MLC and LPS-induced vascular hyperpermeability. Taken together, Wogonin can inhibit LPS-induced vascular permeability by suppressing the MLCK/MLC pathway, suggesting a therapeutic potential for the diseases associated with the development of both inflammatory and tumor.

Description

Wogonin is a cell-permeable and orally available flavonoid that displays anti-inflammatory and anticancer properties.

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