|Source:||The herbs of Scutellaria baicalensis Georgi.|
|Biological Activity or Inhibitors:||1. Wogonoside has anti-inflammatory effect, via dual inhibition of NF-κB and NLRP3 inflammasome.
2. Wogonoside led to reduced Bcl-2 expression and increased Bax expression, while as it led to s decrease in the levels of mitochondrial cytochrome c and an increase in cytosolic fraction and expressions of cytosolic apoptotic protease activating factor-1 (Apaf-1).
3. Wogonoside has shown preclinical anticancer efficacy in various cancer models.
|Solvent:||Pyridine, Methanol, Ethanol, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: firstname.lastname@example.org
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||2.1721 mL||10.8604 mL||21.7207 mL||43.4414 mL||54.3018 mL|
|5 mM||0.4344 mL||2.1721 mL||4.3441 mL||8.6883 mL||10.8604 mL|
|10 mM||0.2172 mL||1.086 mL||2.1721 mL||4.3441 mL||5.4302 mL|
|50 mM||0.0434 mL||0.2172 mL||0.4344 mL||0.8688 mL||1.086 mL|
|100 mM||0.0217 mL||0.1086 mL||0.2172 mL||0.4344 mL||0.543 mL|
Biochem Pharmacol. 2015 Mar 15;94(2):142-54.
|Wogonoside protects against dextran sulfate sodium-induced experimental colitis in mice by inhibiting NF-κB and NLRP3 inflammasome activation.[Pubmed: 25677765]|
|Previous studies have demonstrated that Wogonoside, the glucuronide metabolite of wogonin, has anti-inflammatory, anti-angiogenic and anticancer effects. However, the anti-inflammatory mechanism of Wogonoside has not been fully elucidated. Recently, NLRP3 inflammasome has been reported to be correlated with inflammatory bowel disease for its ability to induce IL-1β release. Nevertheless, there are few drug candidates targeting NLRP3 inflammasome for this disease. In this study, we investigated the anti-inflammatory effect of Wogonoside in dextran sulfate sodium (DSS)-induced murine colitis and further revealed the underlying mechanisms by targeting NF-κB and NLRP3 inflammasome. Wogonoside treatment dose-dependently attenuated DSS-induced body weight loss and colon length shortening. Moreover, Wogonoside prevented DSS-induced colonic pathological damage, remarkably inhibited inflammatory cells infiltration and significantly decreased myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) activities. The production of pro-inflammatory mediators in serum and colon was also significantly reduced by Wogonoside. The underlying mechanisms for the protective effect of Wogonoside in DSS-induced colitis may be attributed to its inhibition on NF-κB and NLRP3 inflammasome activation in colons. Furthermore, Wogonoside markedly decreased production of IL-1β, TNF-α and IL-6 and suppressed mRNA expression of pro-IL-1β and NLRP3 in phorbol myristate acetate (PMA)-differentiated monocytic THP-1 cells via inhibiting the activation of NF-κB and NLRP3 inflammasome. In conclusion, our study demonstrated that Wogonoside may exert its anti-inflammatory effect via dual inhibition of NF-κB and NLRP3 inflammasome, suggesting that Wogonoside might be a potential effective drug for inflammatory bowel diseases.|
Int J Clin Exp Pathol. 2015 Jan 1;8(1):63-72. eCollection 2015.
|Wogonoside induces cell cycle arrest and mitochondrial mediated apoptosis by modulation of Bcl-2 and Bax in osteosarcoma cancer cells.[Pubmed: 25755693]|
|Osteosarcoma (OS) is the most common bone cancer with a great tendency for local invasion and distant metastasis. Restricted by the severe toxicity of conventional drugs, the therapeutic challenge of osteosarcoma still remains unconquered. The objective of the present research work was to investigate the antiproliferative activity of Wogonoside against human osteosarcoma (SaOS-2) cell line. Cell viability after Wogonoside treatment was evaluated by MTT assay. Phase contrast microscopy was used to evaluate the change in cell morphology following drug treatment. The effect of Wogonoside on cell cycle phase distribution and mitochondrial membrane potential was investigated by flow cytometry using propidium iodide (PI) and rhodamine-123 DNA-binding fluorescent dyes respectively. Western blotting was used to evaluate the effect of Wogonoside on cell cycle-related proteins as well as on the expression levels of Bcl-2, Bax, cytosolic and mitochondrial cytochrome c and apoptotic protease activating factor-1 (Apaf-1). Wogonoside induced a dose-dependent as well as time-dependent growth inhibitory effects on cell proliferation of SaOS-2 cancer cells. Wogonoside induced G2/M cell cycle arrest as well as loss in mitochondrial membrane potential in these cells. Within 48 h of incubation, approximately 4.36%, 6.72%, 11.54%, 21.88% and 15.54% of the cells underwent early apoptosis after treatment with 0, 5, 10, 25 and 75 μM of Wogonoside respectively. Wogonoside led to reduced Bcl-2 expression and increased Bax expression, while as it led to s decrease in the levels of mitochondrial cytochrome c and an increase in cytosolic fraction and expressions of cytosolic apoptotic protease activating factor-1 (Apaf-1).|
Oncol Rep. 2014 Sep;32(3):1179-87.
|Wogonoside induces autophagy-related apoptosis in human glioblastoma cells.[Pubmed: 24970553]|
|Wogonoside, a bioactive flavonoid extracted from the root of Scutellaria baicalensis Georgi, has shown preclinical anticancer efficacy in various cancer models. However, the effects of Wogonoside on glioblastoma cells remain unclear. In the present study, we found that Wogonoside exhibited a cytotoxic effect on human glioblastoma cells. The suppression of cell viability was due to the induction of mitochondrial apoptosis. Furthermore, the presence of autophagic hallmarks, including an increase in punctate microtubule associated protein 1 light chain 3 (LC3) dots, changes in cellular morphology and increased levels of autophagy-related proteins were observed in the Wogonoside-treated cells. Wogonoside treatment also enhanced autophagic flux as reflected by the increased acidic vesicular organelle (AVO) formation, p62 degradation and LC3 turnover. Notably, blockade of autophagy by a chemical inhibitor or RNA interference decreased the anticancer effect of Wogonoside. In addition, the p38 mitogen-activated protein kinase (MAPK) signaling pathway, the phosphatidylinositide 3-kinase/protein kinase B/mammalian target of rapamycin/p70S6 kinase (PI3K/AKT/mTOR/p70S6K) signaling pathway and reactive oxygen species (ROS) participated in Wogonoside-induced autophagy and apoptosis. These findings support the initiation of further studies of Wogonoside as a candidate for the treatment of human malignant glioma.|
Inflammation. 2014 Dec;37(6):2006-12.
|Wogonoside ameliorates lipopolysaccharide-induced acute lung injury in mice.[Pubmed: 24854163]|
|Wogonoside has been reported to have anti-inflammatory properties. In this study, we evaluated the effect of Wogonoside on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Male BALB/c mice with ALI, induced by intranasal instillation of LPS, were treated with Wogonoside 1 h prior to LPS exposure. Mice treated with LPS alone showed significantly increased TNF-α, IL-6, and IL-1β levels in the bronchoalveolar lavage fluid (BALF). When pretreated with Wogonoside, the TNF-α, IL-6, and IL-1β levels were significantly decreased. Meanwhile, Wogonoside significantly inhibited LPS-induced increases in the macrophage and neutrophil infiltration of lung tissues and markedly attenuated myeloperoxidase activity. Furthermore, Wogonoside inhibited the TLR4 expression and the phosphorylation of NF-κB p65, and IκB induced by LPS. In conclusion, our results indicate that Wogonoside exhibits a protective effect on LPS-induced ALI via suppression of TLR4-mediated NF-κB signaling pathways.|