|Source:||The herbs of Linaria vulgaris|
|Biological Activity or Inhibitors:||1. Liriodendrin has anti-inflammatory and antinociceptive activities.
2. Liriodendrin shows an excellent hypoglycemic activity.
3. Liriodendrin has protective effects on dopamine-induced cytotoxicity via its anti-oxidative properties by reducing ROS level and anti-apoptotic effect via protection of mitochondrion membrane potential (ΔΨm).
4. Liriodendrin may be a potent suppressor of CaCl(2)-induced arrhythmias, the prophylactic administration of liriodendrin is effective in prolonging latency of arrhythmia and reducing the occurrence of ventricular fibrillation from 75% to 25%.
5. Liriodendrin has inhibitory activities on gastritis and gastric ulcer, it can inhibit colonization of Helicobacter pylori effectively, it could be utilized for the treatment and/or protection of gastritis and gastric ulcer.
6. Liriodendrin plays protective role in sepsis-induced acute lung injury, it regulates lung inflammation, the phosphorylation of the NF-kB (p65) and expression of vascular endothelial growth factor (VEGF).
|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||1.3464 mL||6.7322 mL||13.4644 mL||26.9288 mL||33.661 mL|
|5 mM||0.2693 mL||1.3464 mL||2.6929 mL||5.3858 mL||6.7322 mL|
|10 mM||0.1346 mL||0.6732 mL||1.3464 mL||2.6929 mL||3.3661 mL|
|50 mM||0.0269 mL||0.1346 mL||0.2693 mL||0.5386 mL||0.6732 mL|
|100 mM||0.0135 mL||0.0673 mL||0.1346 mL||0.2693 mL||0.3366 mL|
Biomol Ther (Seoul). 2015 Jan;23(1):53-9.
|Protective Effect of Liriodendrin Isolated from Kalopanax pictus against Gastric Injury.[Pubmed: 25593644]|
|In this study, we investigated the inhibitory activities on gastritis and gastric ulcer using Liriodendrin which is a constituent isolated from Kalopanax pictus. To elucidate its abilities to prevent gastric injury, we measured the quantity of prostaglandin E2 (PGE2) as the protective factor, and we assessed inhibition of activities related to excessive gastric acid be notorious for aggressive factor and inhibition of Helicobacter pylori (H. pylori) colonization known as a cause of chronic gastritis, gastric ulcer, and gastric cancer. Liriodendrin exhibited higher PGE2 level than rebamipide used as a positive control group at the dose of 500 μM. It was also exhibited acid-neutralizing capacity (10.3%) and H(+)/K(+)-ATPase inhibition of 42.6% (500 μM). In pylorus-ligated rats, Liriodendrin showed lower volume of gastric juice (4.38 ± 2.14 ml), slightly higher pH (1.53 ± 0.41), and smaller total acid output (0.47 ± 0.3 mEq/4 hrs) than the control group. Furthermore Liriodendrin inhibited colonization of H. pylori effectively. In vivo test, Liriodendrin significantly inhibited both of HCl/EtOH-induced gastritis (46.9 %) and indomethacin-induced gastric ulcer (46.1%). From these results, we suggest that Liriodendrin could be utilized for the treatment and/or protection of gastritis and gastric ulcer.|
Arch Pharm Res. 2010 Dec;33(12):1927-32.
|A new triterpene and an antiarrhythmic liriodendrin from Pittosporum brevicalyx.[Pubmed: 21191756]|
|A new triterpene, 21-O-senecioyl-R(1)-barrigenol (1) and 13 known compounds were isolated from the ethanol extracts of the leaves and bark of Pittosporum brevicalyx (Oliv.) Gagnep. Their structures were elucidated based on spectral data. The antiarrhythmic action of one furofuran lignan, Liriodendrin (2), was tested on a model of CaCl(2)-induced arrhythmia and compared with the effect of verapamil. The prophylactic administration of Liriodendrin (2) was effective in prolonging latency of arrhythmia and reducing the occurrence of ventricular fibrillation from 75% to 25%. The overall mortality rate was significantly reduced by the prophylactic administration of Liriodendrin from 87.5% to 25%. The antiarrhythmic effect of Liriodendrin (5.0 mg/kg) was similar to that of verapamil (1.05 mg/kg). Thus, Liriodendrin may be a potent suppressor of CaCl(2)-induced arrhythmias.|
Planta Med. 2003 Jul;69(7):610-6.
|In vivo anti-inflammatory and antinociceptive effects of liriodendrin isolated from the stem bark of Acanthopanax senticosus.[Pubmed: 12898415]|
|In the present study, Liriodendrin isolated by activity-guided fractionation from the ethyl acetate (EtOAc) extracts of the stem bark of Acanthopanax senticosus, was evaluated for anti-inflammatory and antinociceptive activities. Liriodendrin (5, 10 mg/kg/day, p. o.) significantly inhibited the increase of vascular permeability induced by acetic acid in mice and reduced an acute paw edema induced by carrageenan in rats. When the analgesic activity was measured by the acetic acid-induced writhing test and hot plate test, Liriodendrin showed a dose-dependent inhibition in animal models. In addition, syringaresinol, the hydrolysate of Liriodendrin, more potently inhibited the LPS-induced production of NO, PGE 2 and TNF-alpha production of macrophages than Liriodendrin. Consistent with these observations, the expression level of iNOS and COX-2 enzyme was decreased by syringaresinol in a concentration-dependent manner. These results suggest that the anti-inflammatory and antinociceptive effects of Liriodendrin after oral administration were attributable to the in vivo transformation to syringaresinol, which may function as the active constituent.|
Arch Pharm Res. 1999 Feb;22(1):30-4.
|Metabolism of liriodendrin and syringin by human intestinal bacteria and their relation to in vitro cytotoxicity.[Pubmed: 10071956]|
|When Liriodendrin or syringin was incubated for 24 h with human intestinal bacteria, two metabolites, (+)-syringaresinol-beta-D-glucopyranoside and (+)-syringaresinol, from Liriodendrin and one metabolite, synapyl alcohol, from syringin were produced. The metabolic time course of Liriodendrin was as follows: at early time, Liriodendrin was converted to (+)-syringaresinol-beta-D-glucopyranoside, and then (+)-syringaresinol. The in vitro cytotoxicities of these metabolites, (+)-syringaresinol and synapyl alcohol, were superior to those of Liriodendrin and syringin.|
Journal of Chinese Pharmaceutical Sciences, 2007, 16(4):294-9.
|Liriodendrin protects SH-SY5Y cells from dopamine-induced cytotoxicity.[Reference: WebLink]|
|To investigate the effect of Liriodendrin, an extract from Fraxinus sielboldiana blume belonging to the Oleaceae family, on dopamine-induced cytotoxicity in human neuroblastoma SH-SY5Y cells. Methods Cell viability was processed when treated with 50μmol·L–1 of dopamine for 24 h by MTT assay. Early apoptosis, late apoptosis/necrosis were analyzed by flow cytometry using Annexin V-FITC and propidium iodide (PI) double-staining, respectively. Generation of reactive oxygen species (ROS) was assessed by DCFH-DA, an oxidation-sensitive fluorescent probe. To evaluate mitochondrion membrane potential (ΔΨm) using flow cytometry with the fluorescent dye Rhodamine 123. The transcriptional level of P53 was studied using RT- PCR. Results The dopamine-induced loss of cell viability was significantly attenuated by Liriodendrin treatment at the concentra- tion of 10–8, 10–7, 10–6, 10–5 and 10–4 mol·L–1. The protective effects of Liriodendrin (10–7, 10–6 and 10–5 mol·L–1) on dopamine-in- duced cytotoxicity may be ascribed to its anti-oxidative properties by reducing ROS level and anti-apoptotic effect via protection of ΔΨm. In addition, the effect of Liriodendrin may involve the P53 pathway in apoptosis. Conclusion Liriodendrin may provide a useful therapeutic strategy for the treatment of neurodegenerative diseases such as Parkinson’s disease (PD).|
Medical Journal of Wuhan University, 2008, 29(6):759-62.
|Hypoglycemic Effects of Active Constituents Extracted from the Stem Bark of Kalopanax Septemlobus(Thunb.)Koidz.in Guangxi.[Reference: WebLink]|
|To study the hypoglycemic active fractions or constituents that were extracted and isolated from the stem bark of Kalopanax septemlobus(Thunb.) Koidz.in Guangxi.Methods: Three fractions were obtained by extracting with alcohol,separating systematically and isolating by the silica and macroporous resin chromatography methods.The hypoglycemic activity of the constituents from the three fractions respectively was evaluated using diabetic models induced by alloxanin in mice.Then the effective fraction was separated by pharmacodynamic test and the monomer components were identified from the effective fraction.Results: Three monomer components,Liriodendrin(Ⅰ),Kalopanax saponine B(Ⅱ) and Kalopanax saponine H(Ⅲ),were obtained from the only effective fraction of all the three fractions.Conclusion: Liriodendrin(Ⅰ) is thought to be found firstly in this plant,and the fraction extracted from Kalopanax septemlobus(Thunb.) Koidz.in Guangxi showes an excellent hypoglycemic activity.|
Inflammation. 2016 Oct;39(5):1805-13.
|Protective Role of Liriodendrin in Sepsis-Induced Acute Lung Injury.[Pubmed: 27498121]|
|In current study, we investigated the role of Liriodendrin, a constituent isolated from Sargentodoxa cuneata (Oliv.) Rehd. Et Wils (Sargentodoxaceae), in cecal ligation and puncture (CLP)-induced acute lung inflammatory response and injury (ALI). The inflammatory mediator levels in bronchoalveolar lavage fluid (BALF) were determined by enzyme-linked immunosorbent assay (ELISA). Pathologic changes in lung tissues were evaluated via pathological section with hematoxylin and eosin (H&E) staining. To investigate the mechanism whereby Liriodendrin regulates lung inflammation, the phosphorylation of the NF-kB (p65) and expression of vascular endothelial growth factor (VEGF) were determined by western blot assay. We show that Liriodendrin treatment significantly improved the survival rate of mice with CLP-induced sepsis. Pulmonary histopathologic changes, alveolar hemorrhage, and neutrophil infiltration were markedly decreased by Liriodendrin. In addition, Liriodendrin decreased the production of the proinflammatory mediators including (TNF-α, IL-1β, MCP-1, and IL-6) in lung tissues. Vascular permeability and lung myeloperoxidase (MPO) accumulation in the Liriodendrin-treated mice were substantially reduced. Moreover, Liriodendrin treatment significantly suppressed the expression of VEGF and activation of NF-kB in the lung. We further show that Liriodendrin significantly reduced the production of proinflammatory mediators and downregulated NF-kB signaling in LPS-stimulated RAW 264.7 macrophage cells. Moreover, Liriodendrin prevented the generation of reactive oxygen species (ROS) by upregulating the expression of SIRT1 in RAW 264.7 cells. These findings provide a novel theoretical basis for the possible application of Liriodendrin in clinic.|