|Description:||1. Vitexin-induced antitumor effect and cytotoxic activity is exerted through proapoptotic process, which is mediated by a decreased Bcl-2/Bax ratio and activation of caspases. |
2. Vitexin and isovitexin have inhibitory effect on the formation of advanced glycation endproducts, the anti-glycation activities may mainly be due to their free radical scavenging capacity.
3. Vitexin can be effectively used for the prevention of UV-induced adverse skin reactions such as free radical production and skin cell damage.
4. Vitexin has spasmolytic effects, because it non-competitively inhibits Ach but not the Ca(2+) influx.
5. Vitexin, an HIF-1alpha inhibitor, it has anti-metastatic potential in PC12 cells.
6. Vitexin has anti-inflammatory and antinociceptive activities, it can inhibit inflammatory pain in mice by targeting TRPV1, oxidative stress, and cytokines.
7. Vitexin protects brain against ischemia/reperfusion injury via modulating mitogen-activated protein kinase and apoptosis signaling in mice.
8. Vitexin has anticonvulsant effects in the brain, possibly through interaction at the benzodiazepine site of the γ-aminobutyric acid type A receptor complex.
9. Vitexin has anti-depressant effects, the mechanism is mediated through an increase in catecholamine levels in the synaptic cleft as well as through interactions with the serotonergic 5-HT1A , noradrenergic α2 , and dopaminergic D1 , D2 , and D3 receptors.
|Targets:||5-HT Receptor | P450 (e.g. CYP17) | ERK | JNK | Bcl-2/Bax | p38MAPK | TRPV | TNF-α | IL Receptor | HIF | VEGFR | Calcium Channel|
|Source:||The seeds of Vitex trifolia L.|
|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.
Need more advice on solubility, usage and handling? Please email to: email@example.com
|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||2.3127 mL||11.5634 mL||23.1267 mL||46.2535 mL||57.8168 mL|
|5 mM||0.4625 mL||2.3127 mL||4.6253 mL||9.2507 mL||11.5634 mL|
|10 mM||0.2313 mL||1.1563 mL||2.3127 mL||4.6253 mL||5.7817 mL|
|50 mM||0.0463 mL||0.2313 mL||0.4625 mL||0.9251 mL||1.1563 mL|
|100 mM||0.0231 mL||0.1156 mL||0.2313 mL||0.4625 mL||0.5782 mL|
Eur J Pharmacol. 2013 Jan 15;699(1-3):250-7.
|Anti-depressant-like effect of vitexin in BALB/c mice and evidence for the involvement of monoaminergic mechanisms.[Pubmed: 23099258 ]|
|The anti-immobility effect of Vitexin in the tail-suspension test was reversed with α-methyl-para-tyrosine methyl ester (AMPT, an inhibitor of catecholamine synthesis, 100mg/kg, i.p.), yohimbine (an α(2)-adrenoceptor antagonist, 1mg/kg, i.p.), NAN 190 (a 5-HT(1A) antagonist, 0.5mg/kg, i.p.), SCH 23390 (a dopamine D(1) antagonist, 0.05 mg/kg, s.c.) and sulpiride (a dopamine D(2)/D(3) antagonist, 50mg/kg, i.p.). The same effect was not reversed, however, by p-chlorophenylalanine methyl ester (PCPA; an inhibitor of serotonin synthesis 100mg/kg, i.p., administered for 4 consecutive days), ketanserin (a 5-HT(2A/2C) antagonist, 1-4 mg/kg, i.p.), ondansetron (a 5-HT(3) antagonist, 0.1-0.4 mg/kg, i.p.), prazosin (an α(1)-adrenoceptor antagonist, 1-4 mg/kg, i.p.), or propranolol (a non-selective β-adrenoceptor antagonist, 5-20mg/kg, i.p.). These results suggest that the anti-depressant-like effect of Vitexin is mediated through an increase in catecholamine levels in the synaptic cleft as well as through interactions with the serotonergic 5-HT(1A), noradrenergic α(2), and dopaminergic D(1), D(2), and D(3) receptors. To our knowledge, this is the first study to show findings that indicate an anti-depressant-like effect of Vitexin and its underlying mechanisms.|
Phytomedicine. 2015 Mar 15;22(3):379-84.
|Vitexin protects brain against ischemia/reperfusion injury via modulating mitogen-activated protein kinase and apoptosis signaling in mice.[Pubmed: 25837275]|
|Vitexin is a major bioactive flavonoid compound derived from the dried leaf of hawthorn (Crataegus pinnatifida), a widely used conventional folk medicine in China. Recent studies have shown that Vitexin presents neuroprotective effects in vitro. Whether this protective effect applies to the cerebral ischemia/reperfusion (I/R) injury remains elusive. In the present study, we examined the potential neuroprotective effect of Vitexin against cerebral I/R injury and underlying mechanisms. A focal cerebral I/R model in male Kunming mice was induced by middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion for 22 h. The neurological function and infarct volume were assessed by using Long's five-point scale system and triphenyl-tetrazolium chloride (TTC) staining technique, respectively. Neuronal damage was evaluated by histological staining. Extracellular signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinases (JNK) and p38 phosphorylation, and apoptosis were measured via Western blot at 24 h after reperfusion. As a result, systemic Vitexin treatment significantly reduced neurological deficit, cerebral infarct volume and neuronal damage when compared with the I/R group. Western blot analyses revealed that Vitexin markedly upregulated p-ERK1/2 and downregulated p-JNK and p-p38. Meanwhile, Vitexin increased Bcl-2 expression and suppressed the overexpression of Bax in the I/R injury mice. In conclusion, the results indicate that Vitexin protects brain against cerebral I/R injury, and this effect may be regulated by mitogen-activated protein kinase (MAPK) and apoptosis signaling pathways.|
Chem Biol Drug Des. 2012 Aug;80(2):274-8.
|Neuroprotective effects of vitexin, a flavonoid, on pentylenetetrazole-induced seizure in rats.[Pubmed: 22554436]|
|Flavonoids are important constituents of food and beverages and have several neuropharmacological activities. Many of these compounds are ligands for γ-aminobutyric acid type A receptors in the central nervous system. This study aimed to investigate the anticonvulsant effects of intracerebroventricularly administered Vitexin (5, 7, 4-trihydroxyflavone-8-glucoside), a flavonoid found in plants, in rats treated with pentylenetetrazole (90 mg/kg, intraperitoneally) and to clarify the underlying mechanism. Vitexin (100 and 200 μm, i.c.v) affected minimal clonic seizures and generalized tonic-clonic seizures induced by pentylenetetrazole by increasing the seizure onset time. Pretreatment with flumazenil suppressed the anticonvulsant effects of Vitexin during the onset of both the seizures. These results indicate that Vitexin has anticonvulsant effects in the brain, possibly through interaction at the benzodiazepine site of the γ-aminobutyric acid type A receptor complex.|
J Nat Prod. 2013 Jun 28;76(6):1141-9.
|Vitexin inhibits inflammatory pain in mice by targeting TRPV1, oxidative stress, and cytokines.[Pubmed: 23742617]|
|The flavonoid Vitexin (1) is a flavone C-glycoside (apigenin-8-C-β-D-glucopyranoside) present in several medicinal and other plants. Plant extracts containing 1 are reported to possess antinociceptive, anti-inflammatory, and antioxidant activities. However, the only evidence that 1 exhibits antinociceptive activity was demonstrated in the acetic acid-induced writhing model. Therefore, the analgesic effects and mechanisms of 1 were evaluated. In the present investigation, intraperitoneal treatment with 1 dose-dependently inhibited acetic acid-induced writhing. Furthermore, treatment with 1 also inhibited pain-like behavior induced by phenyl-p-benzoquinone, complete Freund's adjuvant (CFA), capsaicin (an agonist of transient receptor potential vanilloid 1, TRPV1), and both phases of the formalin test. It was also observed that inhibition of carrageenan-, capsaicin-, and chronic CFA-induced mechanical and thermal hyperalgesia occurred. Regarding the antinociceptive mechanisms of 1, it prevented the decrease of reduced glutathione levels, ferric-reducing ability potential, and free-radical scavenger ability, inhibited the production of hyperalgesic cytokines such as TNF-α, IL-1β, IL-6, and IL-33, and up-regulated the levels of the anti-hyperalgesic cytokine IL-10. These results demonstrate that 1 exhibits an analgesic effect in a variety of inflammatory pain models by targeting TRPV1 and oxidative stress and by modulating cytokine production.|
Mol Cells. 2006 Dec 31;22(3):291-9.
|Vitexin, an HIF-1alpha inhibitor, has anti-metastatic potential in PC12 cells.[Pubmed: 17202857]|
|Vitexin, a natural flavonoid compound identified as apigenin-8-C-b-D-glucopyranoside, has been reported to exhibit antioxidative and anti-inflammatory properties. In this study, we investigated its effect on hypoxia-inducible factor-1a (HIF-1a) in rat pheochromacytoma (PC12), human osteosarcoma (HOS) and human hepatoma (HepG2) cells. Vitexin inhibited HIF-1a in PC12 cells, but not in HOS or HepG2 cells. In addition, it diminished the mRNA levels of hypoxia-inducible genes such as vascular endothelial growth factor (VEGF), smad3, aldolase A, enolase 1, and collagen type III in the PC12 cells. We found that Vitexin inhibited the migration of PC12 cells as well as their invasion rates, and it also inhibited tube formation by human umbilical vein endothelium cells (HUVECs). Interestingly, Vitexin inhibited the hypoxia-induced activation of c-jun N-terminal kinase (JNK), but not of extracellular-signal regulated protein kinase (ERK), implying that it acts in part via the JNK pathway. Overall, these results suggest the potential use of Vitexin as a treatment for diseases such as cancer.|
J Ethnopharmacol. 2007 Sep 5;113(2):258-66.
|The spasmolytic effect of Aloysia citriodora, Palau (South American cedrón) is partially due to its vitexin but not isovitexin on rat duodenums.[Pubmed: 17640836 ]|
|Two flavonoids were identified by HPLC in the AEC: Vitexin and isoVitexin. Vitexin non-competitively inhibited the Ach-DRC (pD(2') of 5.7 +/- 0.4) but significantly run leftward the DRC of Ca(2+). IsoVitexin did not significantly inhibit the DRC of Ach nor Ca(2+). The results suggest that the spasmolytic effect of AEC could be mostly associated to the increase in cGMP (target shared with the PDE inhibitors) and the activation of K(+)-channels. At low concentrations, AEC also inhibits the aerobic metabolism. The flavonoid Vitexin is partially responsible for the effect, since it non-competitively inhibits Ach but not the Ca(2+) influx. IsoVitexin was devoid of activity on duodenums.|
Arch Pharm Res. 2005 Feb;28(2):195-202.
|The isolation and antioxidative effects of vitexin from Acer palmatum.[Pubmed: 15789751]|
|The biological activities of Vitexin were investigated for the potential application of its anti-aging effects in the cosmetic field. Vitexin inhibited superoxide radicals by about 70% at a concentration of 100 microg/mL and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals by about 60% at a concentration of 100 microg/mL. Intracellular ROS scavenging activity was indicated by increases in dichlorofluorescein (DCF) fluorescence upon exposure to UVB 20 mJ/cm2 in cultured human dermal fibroblasts (HDFs) after the treatment of Vitexin. The results show that oxidation of 5-(6-)chloromethyl-2',7'-dichlorodihydrofluorescein diacetate (CM-H2DCFDA) is inhibited by Vitexin effectively and that Vitexin has a potent free radical scavenging activity in UVB-irradiated HDFs. In ROS imaging using a confocal microscope we visualized DCF fluorescence in HDFs directly. In conclusion, our findings suggest that Vitexin can be effectively used for the prevention of UV-induced adverse skin reactions such as free radical production and skin cell damage.|
Food Chem., 2008, 106(2):475-81.
|Inhibitory effect of mung bean extract and its constituents vitexin and isovitexin on the formation of advanced glycation endproducts.[Reference: WebLink]|
|Subsequent HPLC analysis of mung bean extract revealed two major phenolics which were purified and identified as Vitexin and isoVitexin by spectral methods. In the anti-glycation assays, both Vitexin and isoVitexin showed significant inhibitory activities against the formation of AGEs induced by glucose or methylglyoxal with efficacies of over 85% at 100 μM. In another assay, Vitexin and isoVitexin failed to directly trap reactive carbonyl species, such as methylglyoxal, suggesting that their anti-glycation activities may mainly be due to their free radical scavenging capacity.|
Clin Cancer Res. 2009 Aug 15;15(16):5161-9.
|Vitexins, nature-derived lignan compounds, induce apoptosis and suppress tumor growth.[Pubmed: 19671865]|
|Contrasts to the classic lignans, Vitexins were not metabolized to END and ENL. A mixture of Vitexins EVn-50 and purified Vitexin compound 6-hydroxy-4-(4-hydroxy-3-methoxyphenyl)-3-hydroxymethyl-7-methoxy-3, 4-dihydro-2-naphthaldehyde have cytotoxic effect on breast, prostate, and ovarian cancer cells and induces apoptosis with cleavage in poly ADP ribose polymerase protein, up-regulation of Bax, and down-regulation of Bcl-2. This induction of apoptosis seems to be mediated by activation of caspases because inhibition of caspases activity significantly reduced induced apoptosis. We showed a broad antitumor activity of EVn-50 on seven tumor xenograft models including breast, prostate, liver, and cervical cancers. Consistent with in vitro data, EVn-50 treatment induced apoptosis, down-regulated of Bcl-2, and up-regulated Bax in tumor xenografts. CONCLUSION: Vitexin is a class of nature lignan compounds, whose action and anticancer effect is mediated by the mechanisms different from the classic lignans. Vitexin-induced antitumor effect and cytotoxic activity is exerted through proapoptotic process, which is mediated by a decreased Bcl-2/Bax ratio and activation of caspases.|