|Source:||The root of Scutellaria baicalensis Georgi|
|Biological Activity or Inhibitors:||1. Scutellarin attenuates H2O2-induced cytotoxicity, intracellular accumulation of ROS and Ca2+, lipid peroxidation, and loss of MMP and DNA, which may represent the cellular mechanisms for its neuroprotective action.
2. Long-term administration of scutellarin improved the cardiac function of MI rats by inhibiting interstitial fibrosis, and the mechanisms may involve the suppression of pro-fibrotic cytokine TGFβ1 expression and inhibition of p38 MAPK and ERK1/2 phosphorylation.
3. Scutellarin has neuroprotection, the mechanism mediated by inhibition of microglial inflammatory activation.
4. Scutellarin has protective effects for cerebral injury through regulating the expression of NOS isoforms and angiogenic molecules.
|Solvent:||DMSO, 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.
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|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||2.1628 mL||10.8139 mL||21.6277 mL||43.2554 mL||54.0693 mL|
|5 mM||0.4326 mL||2.1628 mL||4.3255 mL||8.6511 mL||10.8139 mL|
|10 mM||0.2163 mL||1.0814 mL||2.1628 mL||4.3255 mL||5.4069 mL|
|50 mM||0.0433 mL||0.2163 mL||0.4326 mL||0.8651 mL||1.0814 mL|
|100 mM||0.0216 mL||0.1081 mL||0.2163 mL||0.4326 mL||0.5407 mL|
J Ethnopharmacol. 2015 Mar 13;162:69-78.
|Biological evaluation and molecular docking of baicalin and scutellarin as Helicobacter pylori urease inhibitors.[Pubmed: 25557028]|
|Scutellarin and Baicalin were non-competitive inhibitors targeting sulfhydryl groups especially Cys321 around the active site of Helicobacter pylori urease, representing potential to be good candidate for future research as urease inhibitor for treatment of Helicobacter pylori infection. Furthermore, our work gave additional scientific support to the use of Scutellaria baicalensis in traditional Chinese medicine (TCM) to treat gastrointestinal disorders.|
Molecules. 2014 Sep 29;19(10):15611-23.
|Anti-fibrosis effect of scutellarin via inhibition of endothelial-mesenchymal transition on isoprenaline-induced myocardial fibrosis in rats.[Pubmed: 25268717]|
|The administration of Scutellarin resulted in a significant improvement in cardiac function and decrease in the cardiac weight indices; reduced fibrous tissue proliferation; reduced levels of type I and III collagen; increased microvascular density; and decreased expression of α-smooth muscle actin and increased expression of CD31, Notch1, Jagged1 and Hes1 in isoprenaline-induced myocardial fibrosis in rats. Our results suggest that Scutellarin prevents isoprenaline-induced myocardial fibrosis via inhibition of cardiac endothelial-mesenchymal transition potentially, which may be associated with the Notch pathway.|
Pharmazie. 2014 Jul;69(7):537-41.
|In vivo effects of scutellarin on the activities of CYP1A2, CYP2C11, CYP2D1, and CYP3A1/2 by cocktail probe drugs in rats.[Pubmed: 25073400]|
|Scutellarin could significantly inhibit CYP1A2, CYP2C11 and CYP3A1/2 activities in rats in vivo, but had no effects on the activity of CYP2D1.|
Life Sci. 2004 Apr 30;74(24):2959-73.
|Protection against hydrogen peroxide-induced cytotoxicity in PC12 cells by scutellarin.[Pubmed: 15051420 ]|
|Vitamin E, a potent antioxidant, was employed as a comparative agent. Preincubation of PC12 cells with Scutellarin prevented cytotoxicity induced by H2O2. Intracellular accumulation of ROS, Ca2+ and products of lipid peroxidation, resulting from H2O2 were significantly reduced by Scutellarin. Incubation of cells with H2O2 caused a marked decrease in MMP, which was significantly inhibited by Scutellarin. PC12 cells treated with H2O2 underwent apoptotic death as determined by flow cytometric assay. The percentage of this H2O2-induced apoptosis in the cells was decreased in the presence of different concentrations of Scutellarin. Scutellarin exhibited significantly higher potency compared to the antioxidant vitamin E. The present findings showed that Scutellarin attenuated H2O2-induced cytotoxicity, intracellular accumulation of ROS and Ca2+, lipid peroxidation, and loss of MMP and DNA, which may represent the cellular mechanisms for its neuroprotective action.|
Br J Pharmacol. 2011 Feb;162(3):688-700.
|Scutellarin alleviates interstitial fibrosis and cardiac dysfunction of infarct rats by inhibiting TGFβ1 expression and activation of p38-MAPK and ERK1/2.[Pubmed: 20942814]|
|Interstitial fibrosis plays a causal role in the development of heart failure after chronic myocardial infarction (MI), and anti-fibrotic therapy represents a promising strategy to mitigate this pathological process. The purpose of this study was to investigate the effect of long-term administration of Scutellarin (Scu) on cardiac interstitial fibrosis of myocardial infarct rats and the underlying mechanisms.The echocardiographic and haemodynamic measurements showed that Scu improved the impaired cardiac function of infarct rats and decreased interstitial fibrosis. Scu inhibited the expression of FN1 and TGFβ1, but produced no effects on inflammatory cytokines (TNFα, IL-1β and IL-6) in the 8 week infarct hearts. Scu inhibited the proliferation and collagen production of cardiac fibroblasts (CFs) and the up-regulation of FN1 and TGFβ1 induced by Ang II. The enhanced phosphorylation of p38-MAPK and ERK1/2 in both infarct cardiac tissue and cultured CFs challenged by Ang II were suppressed by Scu. CONCLUSIONS AND IMPLICATIONS: Long-term administration of Scu improved the cardiac function of MI rats by inhibiting interstitial fibrosis, and the mechanisms may involve the suppression of pro-fibrotic cytokine TGFβ1 expression and inhibition of p38 MAPK and ERK1/2 phosphorylation.|
Pharmacol Res. 2005 Mar;51(3):205-10.
|Effect of scutellarin on nitric oxide production in early stages of neuron damage induced by hydrogen peroxide.[Pubmed: 15661569 ]|
|Results also showed that hydrogen peroxide increased activity of cNOS, which was markedly inhibited by Scutellarin. However, exposure of neuronal cells to hydrogen peroxide did not lead to an increase in iNOS activity. In conclusion, our results suggest that NO production, which increased in early stages of neuron damage induced by hydrogen peroxide can be effectively inhibited by Scutellarin. Moreover, our results indicate that increase in NO production is mediated by cNOS.|