|Source:||The herb of Dracocephalum ruyschiana L.|
|Biological Activity or Inhibitors:||1. Luteolin-7-O-glucoside and luteolin potently strengthen the HO-1-mediated antioxidative potential through the modulation of the Nrf2/MAPK signaling pathways.
2. Luteolin-7-O-glucoside shows protective effects against DOX-induced cardiotoxicity may be related to anti-apoptosis through PTEN/Akt and ERK pathway.
3. Luteolin-7-O-glucoside and luteolin can inhibit lipopolysaccharide-induced inflammatory responses through modulation of NF-κB/AP-1/PI3K-Akt signaling cascades in RAW 264.7 cells.
4. Luteolin-7-O-Glucoside can induce apoptosis by scavenging ROS and suppressing the expression of β-catenin in COLO 320 DM cells and effectively inhibit ACF development in DMH-induced experimental carcinogenesis, Hence it can be a potent anticancer drug for colon carcinogenesis.
5. Luteolin-7-O-glucoside has anti-asthmatic activity, can suppress leukotriene C(4) production and degranulation by inhibiting the phosphorylation of mitogen activated protein kinases and phospholipase Cγ1 in activated mouse bone marrow-derived mast cells.
|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||2.2303 mL||11.1513 mL||22.3025 mL||44.605 mL||55.7563 mL|
|5 mM||0.4461 mL||2.2303 mL||4.4605 mL||8.921 mL||11.1513 mL|
|10 mM||0.223 mL||1.1151 mL||2.2303 mL||4.4605 mL||5.5756 mL|
|50 mM||0.0446 mL||0.223 mL||0.4461 mL||0.8921 mL||1.1151 mL|
|100 mM||0.0223 mL||0.1115 mL||0.223 mL||0.4461 mL||0.5576 mL|
Nutr Cancer. 2011;63(1):130-8.
|Cancer chemopreventive potential of luteolin-7-O-glucoside isolated from Ophiorrhiza mungos Linn.[Pubmed: 21161823 ]|
|The anticarcinogenic potential of the phytocompound Luteolin-7-O-glucoside (LUT7G), isolated from the leaves of Ophiorrhiza mungos Linn, was studied against 4 different cancer cell lines (COLO 320 DM, AGS, MCF-7, and A549) and normal VERO cell line. The ability of LUT7G to induce apoptosis was determined by its antiradical activity, DNA fragmentation, expression of β-catenin, and chemopreventive efficacy in vivo by administering rats with DMH (20 mg/kg b.w., s.c.) for 4 consecutive wk and supplementing with 3 different doses throughout the experimental period of 16 wk. LUT7G scavenged 80% of DPPH radicals generated in vitro at 1000 μM and suppressed the expression of β-catenin to 40% at 120 μM concentrations. LUT7G induced apoptosis by scavenging ROS and suppressing the expression of β-catenin in COLO 320 DM cells and effectively inhibited ACF development in DMH-induced experimental carcinogenesis. Hence LUT7G can be a potent anticancer drug for colon carcinogenesis.|
Food Chem Toxicol. 2014 Mar;65:70-5.
|Luteolin and luteolin-7-O-glucoside strengthen antioxidative potential through the modulation of Nrf2/MAPK mediated HO-1 signaling cascade in RAW 264.7 cells.[Pubmed: 24361407]|
|We evaluated the antioxidative potential of luteolin and Luteolin-7-O-glucoside, glycosidic form of luteolin, against the oxidative damage and compared their antioxidative mechanisms in RAW 264.7 cells. Heme oxygenase-1 (HO-1), one of the phase II enzymes showing an antioxidative activity, was potently induced by luteolin and Luteolin-7-O-glucoside treatment, which was in accordance with the translocated nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) into nucleus. Moreover, luteolin and the Luteolin-7-O-glucoside activated HO-1 expression by p38 and c-Jun NH2-terminal kinase (JNK) regulation. In order to identify the antioxidation potential by HO-1, tert-butyl hydroperoxide (t-BHP)-induced oxidative damage was applied and ameliorated by luteolin and the Luteolin-7-O-glucoside treatment in a dose dependent manner, which was confirmed by HO-1 selective inhibitor and inducer, tin protoporphyrin (SnPP) and cobalt protoporphyrin (CoPP), respectively. Consequently, luteolin and Luteolin-7-O-glucoside potently strengthen the HO-1-mediated antioxidative potential through the modulation of the Nrf2/MAPK signaling pathways.|
Cardiovasc Toxicol. 2015 Mar 1.
|Protection of Luteolin-7-O-Glucoside Against Doxorubicin-Induced Injury Through PTEN/Akt and ERK Pathway in H9c2 Cells.[Pubmed: 25724325]|
|Luteolin-7-O-glucoside (LUTG) was isolated from the plants of Dracocephalum tanguticum Maxim. Previous research has showed that Luteolin-7-O-glucoside pretreatment had a significant protective effect against doxorubicin (DOX)-induced cardiotoxicity by reducing intracellular calcium overload and leakage of creatine kinase and lactate dehydrogenase. But the underlying mechanisms have not been completely elucidated. In the present study, we investigated the effects of Luteolin-7-O-glucoside on H9c2 cell morphology, viability, apoptosis, reactive oxygen species generation, and the mitochondrial transmembrane potentials.These results indicated that the protective effects of Luteolin-7-O-glucoside against DOX-induced cardiotoxicity may be related to anti-apoptosis through PTEN/Akt and ERK pathway.|
Nutr Res Pract. 2013 Dec;7(6):423-9.
|Luteolin and luteolin-7-O-glucoside inhibit lipopolysaccharide-induced inflammatory responses through modulation of NF-κB/AP-1/PI3K-Akt signaling cascades in RAW 264.7 cells.[Pubmed: 24353826]|
|Luteolin is an anti-inflammatory and anti-oxidative agent. In this study, the anti-inflammatory capacity of luteolin and one of its glycosidic forms, Luteolin-7-O-glucoside, were compared and their molecular mechanisms of action were analyzed. In lipopolysaccharide (LPS)-activated RAW 264.7 cells, luteolin more potently inhibited the production of nitric oxide (NO) and prostaglandin E2 as well as the expression of their corresponding enzymes (inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) than Luteolin-7-O-glucoside. The molecular mechanisms underlying these effects were investigated to determine whether the inflammatory response was related to the transcription factors, nuclear factor (NF)-κB and activator protein (AP)-1, or their upstream signaling molecules, mitogen-activated protein kinases (MAPKs) and phosphoinositide 3-kinase (PI3K). Luteolin attenuated the activation of both transcription factors, NF-κB and AP-1, while Luteolin-7-O-glucoside only impeded NF-κB activation. However, both flavonoids inhibited Akt phosphorylation in a dose-dependent manner. Consequently, luteolin more potently ameliorated LPS-induced inflammation than Luteolin-7-O-glucoside, which might be attributed to the differentially activated NF-κB/AP-1/PI3K-Akt pathway in RAW 264.7 cells.|
Biol Pharm Bull. 2011;34(7):1032-6.
|Luteolin-7-O-glucoside suppresses leukotriene C(4) production and degranulation by inhibiting the phosphorylation of mitogen activated protein kinases and phospholipase Cγ1 in activated mouse bone marrow-derived mast cells.[Pubmed: 21720009]|
|In this study, Luteolin-7-O-glucoside (L7G), an herbal medicine isolated from Ailanthus altissima, inhibited 5-lipoxygenase (5-LOX)-dependent leukotriene C(4) (LTC(4)) production in bone marrow-derived mast cells (BMMCs) in a concentration-dependent manner with an IC(50) of 3.0 μM. To determine the action mechanism of L7G, we performed immunoblotting for cytosolic phospholipase A(2) (cPLA(2)) and mitogen-activated protein kinases (MAPKs) following c-kit ligand (KL)-induced activation of BMMCs with or without L7G. Inhibition of LTC(4) production by L7G was accompanied by a decrease in cPLA(2) phosphorylation, which occurred via the extracellular signal-regulated protein kinase-1/2 (ERK1/2) and p38 and c-Jun N-terminal kinase (JNK) pathways. In addition, L7G also attenuated mast cell degranulation in a dose-dependent manner (IC(50), 22.8 μM) through inhibition of phospholipase Cγ1 (PLCγ1) phosphorylation. Our results suggest that the anti-asthmatic activity of L7G may be mediated in part via the inhibition of LTC(4) generation and mast cell degranulation.|