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More articles cited ChemFaces products.
Experimental Parasitology2015 March 24.Cell11 Jan. 2018;Sci Rep. Jan. 2018Aquaculture1 Dec. 2017Food Science and Biotechnology2015 Dec. 31
Journal of Pharmaceutical Analysis2016 May 5; University of Limpopo2016Current Pharmaceutical AnalysisIssue 5, 2017Br J Pharmacol.2018 Mar;Phytochemistry Letters22 Dec. 2016
Sci Rep. 2017 Oct 11;Phytomedicine.2018 Jan 1;Chem Pharm Bull (Tokyo).2017;65(9)Research on Crops.Jun 2017;
Our products had been exported to the following research institutions and universities, And still growing.
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||Honokiol has antibacterial, anti-angiogenesis, antidepressant-like, antioxidant, anti-inflammatory and anti-cancer effects. It inhibited the activation of Akt and enhances the phosphorylation of ERK1/ERK2. It can improve learning, memory impairments and neuroinflammatory processes induced by SCOP in mice, by inhibition of AChE activity.|
||NOS | NO | 5-HT Receptor | cAMP | PGE | COX | ERK | IL Receptor | ROS | TNF-α | Antifection | AChE | Akt|
|J. Biol. Chem., 2003, 278(37):35501-7. |
|Honokiol, a Small Molecular Weight Natural Product, Inhibits Angiogenesis in Vitro and Tumor Growth in Vivo.[Reference: WebLink]|
|Natural products comprise a major source of small molecular weight angiogenesis inhibitors. |
METHODS AND RESULTS:
We have used the transformed endothelial cell line SVR as an effective screen of natural product extracts to isolate anti-angiogenesis and anti-tumor compounds. Aqueous extracts of Magnolia grandiflora exhibit potent activity in our SVR proliferation assays. We found that the small molecular weight compound Honokiol is the active principle of magnolia extract. Honokiol exhibited potent anti-proliferative activity against SVR cells in vitro. In addition, Honokiol demonstrated preferential inhibition of primary human endothelial cells compared with fibroblasts and this inhibition was antagonized by antibodies against TNFα-related apoptosis-inducing ligand. In vivo, Honokiol was highly effective against angiosarcoma in nude mice.
Our preclinical data suggests that Honokiol is a systemically available and non-toxic inhibitor of angiogenesis and should be further evaluated as a potential chemotherapeutic agent.
|Eur J Pharmacol. 2004 Aug 2;496(1-3):189-95. |
|In vitro antibacterial and anti-inflammatory effects of honokiol and magnolol against Propionibacterium sp.[Pubmed: 15288590 ]|
|Honokiol and magnolol, two major phenolic constituents of Magnolia sp., have been known to exhibit antibacterial activities. However, until now, their antibacterial activity against Propionibacterium sp. has not been reported.
METHODS AND RESULTS:
To this end, the antibacterial activities of Honokiol and magnolol were detected using the disk diffusion method and a two-fold serial dilution assay. Honokiol and magnolol showed strong antibacterial activities against both Propionibacterium acnes and Propionibacterium granulosum, which are acne-causing bacteria. The minimum inhibitory concentrations (MIC) of Honokiol and magnolol was 3-4 microg/ml (11.3-15 microM) and 9 microg/ml (33.8 microM), respectively. In addition, the killing curve analysis showed that magnolol and Honokiol killed P. acnes rapidly, with 10(5) organisms/ml eliminated within 10 min of treatment with either 45 microg (169.2 microM) of magnolol or 20 microg (75.2 microM) of Honokiol per ml. The cytotoxic effect of Honokiol and magnolol was determined by a colorimetric (3-(4,5-dimetyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide) (MTT) assay using two animal cell lines, human normal fibroblasts and HaCaT. In this experiment, magnolol exhibited lower cytotoxic effects than Honokiol at the same concentration, but they showed similar cytotoxicity when triclosan was employed as an acne-mitigating agent. In addition, they reduced secretion of interleukin-8 and tumor necrosis factor alpha (TNF-alpha) induced by P. acnes in THP-1 cells indicating the anti-inflammatory effects of them. When applied topically, neither phenolic compound induced any adverse reactions in a human skin primary irritation test.
Therefore, based on these results, we suggest the possibility that magnolol and Honokiol may be considered as attractive acne-mitigating candidates for topical application.
|Prog Neuropsychopharmacol Biol Psychiatry. 2008 Apr 1;32(3):715-25. |
|Antidepressant-like effects of the mixture of honokiol and magnolol from the barks of Magnolia officinalis in stressed rodents.[Pubmed: 18093712 ]|
|Honokiol and magnolol are the main constituents simultaneously identified in the barks of Magnolia officinalis, which have been used in traditional Chinese medicine to treat a variety of mental disorders including depression.
METHODS AND RESULTS:
The mixture of Honokiol and magnolol at 20 and 40 mg/kg significantly attenuated CMS-induced decreases of 5-HT levels in frontal cortex, hippocampus, striatum, hypothalamus and nucleus accumbens. And it markedly increased 5-HIAA levels in frontal cortex, striatum and nucleus accumbens at 40 mg/kg and in frontal cortex at 20 mg/kg in the CMS rats. A subsequent reduction in 5-HIAA/5-HT ratio was found in hippocampus and nucleus accumbens in the CMS rats receiving this mixture. Furthermore, the mixture of Honokiol and magnolol reduced elevated corticosterone concentrations in serum to normalize the hypothalamic-pituitary-adrenal (HPA) hyperactivity in the CMS rats. It also reversed CMS-induced reduction in platelet AC activity, via upregulating the cyclic adenosine monophosphate (cAMP) pathway. These results suggested that the mixture of Honokiol and magnolol possessed potent antidepressant-like properties in behaviors involved in normalization of biochemical abnormalities in brain 5-HT and 5-HIAA, serum corticosterone levels and platelet AC activity in the CMS rats.
Our findings could provide a basis for examining directly the interaction of the serotonergic system, the HPA axis and AC-cAMP pathway underlying the link between depression and treatment with the mixture of Honokiol and magnolol.
||The barks of Magnolia officinalis
||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
||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
||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.
Recent ChemFaces New Products and Compounds
Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals
Cell. 2018 Jan 11;172(1-2):249-261.e12. doi: 10.1016/j.cell.2017.12.019.PMID: 29328914
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.PMID: 29149595
Scientific Reports 2017 Dec 11;7(1):17332.doi: 10.1038/s41598-017-17427-6.PMID: 29230013
Molecules. 2017 Oct 27;22(11). pii: E1829.doi: 10.3390/molecules22111829.PMID: 29077044
J Cell Biochem. 2018 Feb;119(2):2231-2239.doi: 10.1002/jcb.26385. PMID: 28857247
Phytomedicine. 2018 Feb 1;40:37-47. doi: 10.1016/j.phymed.2017.12.030.PMID: 29496173
Calculate Dilution Ratios(Only for Reference)
* Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
|Biomaterials. 2015 Jun;53:274-84. |
|Multifunctional effects of honokiol as an anti-inflammatory and anti-cancer drug in human oral squamous cancer cells and xenograft.[Pubmed: 25890726]|
|The aim of this study was to investigate anti-inflammatory and anti-cancer effects of Honokiol (HK) in two oral squamous cancer cell carcinoma (OSCC) cell lines, HN22 and HSC4, through the regulation of inducible nitric oxide synthase (iNOS) and endoplasmic reticulum resident protein 44 (ERp44).
METHODS AND RESULTS:
Griess assay, zymography, and quantitative PCR were performed to study iNOS expression and subsequent nitric oxide (NO) production in OSCC cell lines.
Liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based proteomic analysis was used to elucidate the proteins associated with ER stress and cellular cytotoxic response induced by Honokiol. Pull-down assay and molecular modeling were performed to better understand how Honokiol interacts with ERp44. In vitro and in vivo experiments in which ERp44 expression was knocked down were performed to better understand the effects of ERp44 on a cellular level and anti-cancer effects of Honokiol. Expression levels of iNOS and subsequent NO secretion were reduced in OSCC cell lines treated with Honokiol. ERp44 was significantly decreased in OSCC cell lines by Honokiol treatment. Honokiol directly bound to ERp44, and ERp44 knock-down significantly inhibited oral cancer cell proliferation and colony formation. Moreover, Honokiol treatment effectively inhibited tumor growth and ERp44 levels in BALB/c nude mice bearing HN22 cell xenografts.
Our findings suggest that Honokiol inhibited inflammation and induced apoptosis by suppressing both iNOS/NO and ERp44 expression in HN22 and HSC4 cells and xenograft tumors, and thus could be a potent anti-inflammatory and anti-cancer drug candidate for human oral cancer treatment.
|Eur J Pharmacol. 2015 Apr 23;760:88-95. |
|Honokiol improves learning and memory impairments induced by scopolamine in mice.[Pubmed: 25912802]|
|Honokiol, a lignan isolated from the bark of Magnolia officinalis, has been reported to ameliorate the learning and memory impairments in senesed (SAMP8) mice. However, whether Honokiol could improve scopolamine (SCOP)-induced learning and memory deficits in mice is still unknown.
METHODS AND RESULTS:
In this study, we aimed to investigate whether Honokiol could reverse the SCOP-induced learning and memory impairments in mice and to elucidate its underlying mechanisms of action. Mice were given daily intraperitoneal injection of Honokiol (10 and 20mg/kg) for 21 consecutive days. The results showed that Honokiol significantly improved spatial learning and memory function (as assessed by the Morris water maze test) in the SCOP-treated mice. In addition, treatment with Honokiol significantly decreased the protein and mRNA levels of interleukin (IL)-1β and the activity of acetylcholinesterase (AChE), while significantly increased the protein and mRNA levels of IL-10, and the level of acetylcholine (Ach) in the brain of the SCOP-treated mice. Moreover, Honokiol also significantly suppressed the production of prostaglandin E 2 (PGE2) and mRNA expression of cyclooxygenase-2 (COX-2) in the brain of the SCOP-treated mice. Mechanistic investigations revealed that Honokiol could markedly reverse the amount of phosphorylated Akt and extracellular regulated kinases 1/2 (ERK1/2) changes in the brain of the SCOP-treated mice.
These results amply demonstrated that Honokiol could improve learning and memory impairments induced by SCOP in mice, and the protective action may be mediated, at least in part, by inhibition of AChE activity, and amelioration of the neuroinflammatory processes in the SCOP-treated mice.
|Brain Res. 2003 Dec 5;992(2):159-66. |
|Honokiol protects rat brain from focal cerebral ischemia-reperfusion injury by inhibiting neutrophil infiltration and reactive oxygen species production.[Pubmed: 14625055]|
|We have previously shown that Honokiol, an active component of Magnolia officinalis, displayed protective effect against focal cerebral ischemia-reperfusion (FCI/R) injury in rats. Production of reactive oxygen species (ROS) and infiltration of neutrophils to injured tissue play deleterious roles during cerebral ischemia. To study the mechanism(s) in mediating neuroprotective effect of Honokiol, FCI/R-induced neutrophil infiltration and lipid peroxidation in brain tissue, and activation of neutrophils in-vitro were examined.
METHODS AND RESULTS:
Intravenous administration of Honokiol (0.01-1.0 microg/kg) 15 min before (pretreatment) or 60 min after (post-treatment) middle cerebral artery occlusion reduced the total infarcted volume by 20-70% in dose-dependent manner. Pretreatment or post-treatment of Honokiol at concentration of 0.1 and 1.0 microg/kg significantly decreased the neutrophil infiltration in the infarcted brain. Time course of neutrophil infiltration was performed in parallel with the lipid peroxidation in infracted brain tissue during FCI/R injury. The results indicate that Honokiol can protect brain tissue against lipid peroxidation and neutrophil infiltration during FCI/R injury and cerebral infarction induced by FCI/R is accompanied with a prominent neutrophil infiltration to the infarcted area during FCI/R course. In-vitro, Honokiol (0.1-10 microM) significantly diminished fMLP (N-formyl-methionyl-leucyl-phenylalanine)- or PMA (phorbol-12-myristate-13-acetate)-induced neutrophil firm adhesion, a prerequisite step behind neutrophil infiltration, and ROS production in neutrophils. Intracellular calcium overloading activates calcium-stimulated enzymes and further exaggerates FCI/R injury. Honokiol (0.1-10 microM) impeded the calcium influx induced by fMLP (a receptor agonist), AlF(4)(-) (a G-protein activator) or thapsigargin (an intracellular calcium pool releaser).
Therefore, we conclude that the amelioration of FCI/R injury by Honokiol can be attributed to its anti-oxidative and anti-inflammatory actions through, at least in part, limiting lipid peroxidation and reducing neutrophil activation/infiltration by interfering firm adhesion, ROS production, and calcium overloading that may be primed/activated during FCI/R injury.