|Source:||The herbs of Prunella vulgaris L.|
|Biological Activity or Inhibitors:||1. Isoquercitrin is a potential stimulator of bone mineralization used for prophylaxis of osteoporotic disorders.
2. Isoquercitrin may be as a potential therapeutic agent against neurodegeneration in Parkinson's disease.
3. Isoquercitrin is an inhibitor of Wnt/β-catenin and may be as a potential novel anti-tumoral agent, such as against human pancreati,liver cancer related to opioid receptors and to the activation of the mitogen-activated protein kinase (MAPK) signalling pathway.
4. Isoquercitrin and quercetin have anti-inflammatory activity in experimental murine allergic asthma, they are effective eosinophilic inflammation suppressors, suggesting a potential for treating allergies.
5. Isoquercitrin has antihypertensive effect, it-induced hypotension in rats is an event dependent on the inhibition of angiotensin II generation by angiotensin converting enzyme (ACE).
6. Isoquercitrin inhibits carbachol and leukotriene D4 -induced contraction in guinea-pig airways, it may be highly useful in treatment of asthma.
|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: 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||2.1533 mL||10.7666 mL||21.5332 mL||43.0663 mL||53.8329 mL|
|5 mM||0.4307 mL||2.1533 mL||4.3066 mL||8.6133 mL||10.7666 mL|
|10 mM||0.2153 mL||1.0767 mL||2.1533 mL||4.3066 mL||5.3833 mL|
|50 mM||0.0431 mL||0.2153 mL||0.4307 mL||0.8613 mL||1.0767 mL|
|100 mM||0.0215 mL||0.1077 mL||0.2153 mL||0.4307 mL||0.5383 mL|
Biochem Pharmacol. 2014 Jun 1;89(3):413-21.
|Isoquercitrin and polyphosphate co-enhance mineralization of human osteoblast-like SaOS-2 cells via separate activation of two RUNX2 cofactors AFT6 and Ets1.[Pubmed: 24726443]|
|Isoquercitrin, a dietary phytoestrogen, is a potential stimulator of bone mineralization used for prophylaxis of osteoporotic disorders. Here we studied the combined effects of Isoquercitrin, a cell membrane permeable 3-O-glucoside of quercetin, and polyphosphate [polyP], a naturally occurring inorganic polymer inducing bone formation, on mineralization of human osteoblast-like SaOS-2 cells. Both compounds Isoquercitrin and polyP induce at non-toxic concentrations the mineralization process of SaOS-2 cells. Co-incubation experiments revealed that Isoquercitrin (at 0.1 and 0.3μM), if given simultaneously with polyP (as Ca(2+) salt; at 3, 10, 30 and 100μM) amplifies the mineralization-enhancing effect of the inorganic polymer. The biomineralization process induced by Isoquercitrin and polyP is based on two different modes of action. After incubation of the cells with Isoquercitrin or polyP the expression of the Runt-related transcription factor 2 [RUNX2] is significantly upregulated. In addition, Isoquercitrin causes a strong increase of the steady-state-levels of the two co-activators of RUNX2, the activating transcription factor 6 [ATF6] and the Ets oncogene homolog 1 [Ets1]. The activating effect of Isoquercitrin occurs via a signal transduction pathway involving ATF6, and by that, is independent from the induction cascade initiated by polyP. This conclusion is supported by the finding that Isoquercitrin upregulates the expression of the gene encoding for osteocalcin, while polyP strongly increases the expression of the Ets1 gene and of the alkaline phosphatase. We show that the two compounds, polyP and Isoquercitrin, have a co-enhancing effect on bone mineral formation and in turn might be of potential therapeutic value for prevention/treatment of osteoporosis.|
Oncol Rep. 2015 Feb;33(2):840-8.
|Isoquercitrin inhibits the progression of pancreatic cancer in vivo and in vitro by regulating opioid receptors and the mitogen-activated protein kinase signalling pathway.[Pubmed: 25434366]|
|Isoquercitrin, which is one of the flavonoids found in Bidens pilosa extracts, has a significant antitumour effect. However, the antitumour effect of Isoquercitrin and its mechanism of action remain unclear. The objective of the present study was to investigate the effect of Isoquercitrin on the progression of pancreatic cancer and to further understand the biological characteristics of the participation of Isoquercitrin in the progression of pancreatic cancer. In vitro, we found that a therapeutic dose of Isoquercitrin significantly inhibited proliferation, promoted apoptosis and induced cell cycle arrest within the G1 phase in pancreatic cancer cells. Isoquercitrin activated caspase-3, -8 and -9 and reduced the mitochondrial membrane potential. In addition, Isoquercitrin inhibited the expression level of the δ opioid receptor; however, Isoquercitrin had no effect on the κ and µ opioid receptors. Furthermore, Isoquercitrin inhibited extracellular signal-regulated kinase (ERK) phosphorylation and promoted c-Jun N-terminal kinase (JNK) phosphorylation. In vivo, we found that a therapeutic dose of Isoquercitrin significantly inhibited xenograft growth in nude mice. In summary, the present study demonstrated that Isoquercitrin inhibits human pancreatic cancer progression in vivo and in vitro and that its molecular mechanism may be closely related to opioid receptors and to the activation of the mitogen-activated protein kinase (MAPK) signalling pathway.|
Oncol Rep. 2014 May;31(5):2377-84.
|Isoquercitrin inhibits the progression of liver cancer in vivo and in vitro via the MAPK signalling pathway.[Pubmed: 24676882]|
|The purpose of the present study was to investigate the impact of Isoquercitrin, the flavonoid from Bidens bipinnata L. extract, on the progression of liver cancer and to achieve a deeper understanding of the biological characteristics of Isoquercitrin's involvement in the progression of liver cancer. In the in vitro experiments, Isoquercitrin was found to strongly inhibit the proliferation of human liver cancer cells, promote the apoptosis of human liver cancer cells, and block the cell cycle in the G1 phase. Isoquercitrin activated caspase-3, -8 and -9, inhibited the expression level of ERK and p38MAPK protein phosphorylation, and promoted the phosphorylation of JNK. Additionally, Isoquercitrin reduced the expression level of PKC in human liver cancer cells. In the in vivo experiments, Isoquercitrin was also found to significantly inhibit the growth of transplanted tumours in nude mice. The present study confirmed that Isoquercitrin could inhibit the progression of human liver cancer in vivo and in vitro, and the molecular mechanism of Isoquercitrin may be closely associated with the MAPK and PKC signalling pathways.|
BMC Res Notes. 2014 Jan 21;7:49.
|Protective effects of flavonol isoquercitrin, against 6-hydroxy dopamine (6-OHDA)-induced toxicity in PC12 cells.[Pubmed: 24443837 ]|
|This study investigated the neuroprotective effects of flavonol Isoquercitrin against toxicity induced by 6-hydroxy-dopamine (6-OHDA) in rat pheochromocytoma (PC12) cells. METHODS: PC12 cells were pretreated with different concentrations of Isoquercitrin for 4, 8 and 12 hours and incubated with 6-OHDA for 24 hours to induce oxidative cell damage. RESULTS: A significant cytoprotective activity was observed in Isoquercitrin pre-treated cells in a dose-dependent manner. There was a significant increase (P < 0.01) in the antioxidant enzymes namely superoxide dismutase, catalase, glutathione peroxidase, and glutathione in Isoquercitrin pretreated cells compared to cells incubated with 6-OHDA alone. Isoquercitrin significantly reduced (P < 0.01) lipid peroxidation in 6-OHDA treated cells. These results suggested that Isoquercitrin protects PC 12 cells against 6-OHDA-induced oxidative stress. CONCLUSIONS: The present study suggests the protective role of Isoquercitrin on 6-hydroxydopamine-induced toxicity by virtue of its antioxidant potential. Isoquercitrin could be a potential therapeutic agent against neurodegeneration in Parkinson's disease.|
J Biol Chem. 2014 Dec 19;289(51):35456-67.
|Isoquercitrin suppresses colon cancer cell growth in vitro by targeting the Wnt/β-catenin signaling pathway.[Pubmed: 25359775]|
|To investigate whether Isoquercitrin affects Wnt/β-catenin signaling. Our data provide strong support for an inhibitory effect of Isoquercitrin on Wnt/β-catenin, where the flavonoid acts downstream of β-catenin translocation to the nuclei. Isoquercitrin affects Xenopus axis establishment, reverses double axes and the LiCl hyperdorsalization phenotype, and reduces Xnr3 expression. In addition, this flavonoid shows anti-tumoral effects on colon cancer cells (SW480, DLD-1, and HCT116), whereas exerting no significant effect on non-tumor colon cell (IEC-18), suggesting a specific effect in tumor cells in vitro. Taken together, our data indicate that Isoquercitrin is an inhibitor of Wnt/β-catenin and should be further investigated as a potential novel anti-tumoral agent.|
Inflamm Res. 2007 Oct;56(10):402-8.
|Anti-inflammatory activity of quercetin and isoquercitrin in experimental murine allergic asthma.[Pubmed: 18026696]|
|Eosinophils and cytokines are implicated in the pathogenesis of allergic diseases. In the present study, we investigate the anti-inflammatory effect of quercetin and Isoquercitrin in a murine model of asthma. METHODS: BALB/c mice were immunized (ovalbumin/aluminum hydroxide, s. c.), followed by two intranasal ovalbumin challenges. From day 18 to day 22 after the first immunization, the mice received daily gavages of Isoquercitrin (15 mg/kg) or quercetin (10 mg/kg). Dexamethasone (1 mg/kg, s. c.) was administered as a positive control. Leucocytes were analyzed in bronchoalveolar lavage fluid (BALF), blood and pulmonary parenchyma at 24 h after the last ovalbumin challenge. Interleukin-5 (IL-5) was analyzed in BALF and lung homogenates. RESULTS: In animals receiving Isoquercitrin or quercetin, eosinophil counts were lower in the BALF, blood and lung parenchyma. Neutrophil counts in blood and IL-5 levels in lung homogenate were lower only in Isoquercitrin-treated mice. No alterations in mononuclear cell numbers were observed. CONCLUSION: Quercetin and Isoquercitrin are effective eosinophilic inflammation suppressors, suggesting a potential for treating allergies.|
J Ethnopharmacol. 2011 Mar 24;134(2):363-72.
|Antihypertensive effects of isoquercitrin and extracts from Tropaeolum majus L.: evidence for the inhibition of angiotensin converting enzyme.[Pubmed: 21185932 ]|
|Previous studies have shown that the extracts obtained from Tropaeolum majus L. exhibit pronounced diuretic properties. In the present study, we assessed whether the hypotensive and/or antihypertensive mechanism of hydroethanolic extract (HETM), semi-purified fraction (TMLR) obtained from T. majus and the flavonoids Isoquercitrin (ISQ) and kaempferol (KPF) can be mediated by their interaction with angiotensin converting enzyme (ACE). METHODS AND METHODS: Firstly, to evaluate changes in mean arterial pressure (MAP), different groups of normotensive and spontaneously hypertensive rats (SHR) were orally and intraduodenally treated with HETM (10-300 mg/kg) and TMLR (12.5-100mg/kg) and intravenously treated with ISQ and KPF being later anesthetized with ketamine (100mg/kg) and xylazine (20mg/kg). The left femoral vein and the right carotid artery were isolated, and polyethylene catheters were inserted for ISQ and KPF (0.5-4 mg/kg) administration and blood pressure recording, respectively. The plasmatic ACE activity was evaluated to indirect fluorimetry, in serum samples after orally treatment with HETM, TMLR, ISQ and KPF. RESULTS: The oral administration of the HETM and its TMLR significantly reduced, in a dose-dependent manner, the MAP in both normotensive and SHR. In addition, these preparations significantly decreased the MAP for up to 3h after the administration of the extract. Additionally, the intravenous administration of ISQ, but not KPF, decreased MAP in rats. Otherwise, neither the extracts nor ISQ affected the heart rate. The oral administration of the HETM, TMLR or ISQ reduced ACE activity in serum samples at 90 min after administration. Finally, the intravenous administration of ISQ caused a significant reduction in the hypertensive response to angiotensin I, but not angiotensin II in normotensive rats. CONCLUSION: Our results show that the hypotensive effects caused by the HETM, as well as by its TMLR, may be associated with the high levels of the flavonoid ISQ found in this plant. In addition, ISQ-induced hypotension in rats is an event dependent on the inhibition of angiotensin II generation by ACE.|
Eur J Pharmacol. 2005 Oct 17;522(1-3):108-15.
|Isoquercitrin from Argemone platyceras inhibits carbachol and leukotriene D4-induced contraction in guinea-pig airways.[Pubmed: 16202993]|
|Argemone platyceras is used in Mexico as a remedy for cough, bronchitis and pneumonia. The present study was performed to investigate the pharmacological anti-asthmatic properties of Argemone platyceras on airways and to identify its active principles. Methanol extracts of leaves and flowers, subsequent organic and aqueous extraction phases, and silica gel chromatography fractions were assayed on the carbachol-induced response, and/or on ovalbumin antigenic challenge, and on leukotriene D(4)-induced response of tracheae from sensitized and non-sensitized guinea-pigs. Methanol extracts, ethyl-acetate phase, and its fractions 6 and 7 inhibited the carbachol-induced contractile response. Isoquercitrin and rutin were the main compounds found in fractions 6 and 7 respectively. Isoquercitrin (fraction 6) abolished the response to ovalbumin, and decreased the contractile response to leukotriene D(4). Because of its effect on carbachol-induced contractile response, on the late-phase response to ovalbumin, and on leukotriene D(4)-induced contractile response, Isoquercitrin might be highly useful in treatment of asthma.|