Editing Magnolia bark extract

[[Information on nutritional supplements people with ALS have been taking]]

[https://en.wikipedia.org/wiki/Magnolia_officinalis Wikipedia page]


== Effects on ALS ==

Magnolol and honokiol are low molecular weight lignans isolated from Magnolia officinalis.

Honokiol is a PPAR-gamma activator {{#pmid:23811337|atanasov2013}} and GABA-alpha receptor agonist {{#pmid:10591411|squires1999}}. PPAR-gamma agonists reduce glutamate release [9] and increase its uptake by astrocytes {{#pmid:17213861|romera2007}}, and increase expression and enzymatic activity of catalase {{#pmid:17213861|romera2007b}}

Honokiol and magnolol potently enhance the potentiating effect of 200 nM GABA on [3H]FNM binding with EC50 values of 0.61 microM and 1.6 microM using rat forebrain membranes, with maximal enhancements of 33 and 47%, respectively. {{#pmid:10591411|squires1999}}

Studies using human U937 promonocytes cells suggested that magnolol differentially down-regulated the pharmacologically induced expression of NF-kappaB-regulated inflammatory gene products MMP-9, IL-8, MCP-1, MIP-1alpha, TNF-alpha. {{#pmid:17240450|tse2007}}

Honokiol significantly enhances ERK1/2 phosphorylation in a concentration-dependent manner {{#pmid:15922325|zhang2005}} and downregulates Klf4 expression in rat spinal cord injury {{#pmid:25774462|liu2015}}.

== Cautions ==

Can slow down the central nervous system, concern that it might slow down the nervous system too much when combined with anesthesia and other medications used during and after surgery. May slow blood clotting and cause bleeding during and after surgery. Interactions with alcohol and sedatives. ([http://www.webmd.com/vitamins-supplements/ingredientmono-188-Magnolia.aspx?activeIngredientId=188&activeIngredientName=Magnolia&source=1 Source: WebMD]). 

On the negative side, honokiol and magnolol enhance TNF induced apoptosis [8].

live casino games online <a href="https://myonlinecasinotop.com/">online casino usa</a> casino game online uk

== Regulated pathways ==

* [http://www.laboratoryequipment.com/news/2015/04/ancient-remedy-may-prevent-reverse-heart-problem?et_cid=4515755&et_rid=281012844&type=cta Upregulates SIRT3 (?)]

* Downregulates MMP-9, IL-8, MCP-1, MIP-1alpha, TNF-alpha.

* Potentiates GABA. 

* Activates PPAR-gamma.

* Enhances TNF induced apoptosis.


== Where to get it ==

* [http://www.amazon.co.uk/dp/B004TSEDKM amazon.co.uk (400 mg capsules)]

== References ==


[8]
<bibtex>
@article{Ahn2006,
abstract = {Recent reports have indicated that honokiol can induce apoptosis, suppress tumor growth, and inhibit angiogenesis. In this report, we found that honokiol potentiated the apoptosis induced by tumor necrosis factor (TNF) and chemotherapeutic agents, suppressed TNF-induced tumor cell invasion, and inhibited RANKL-induced osteoclastogenesis, all of which are known to require nuclear factor-kappaB (NF-kappaB) activation. Honokiol suppressed NF-kappaB activation induced by a variety of inflammatory stimuli, and this suppression was not cell type specific. Further studies showed that honokiol blocked TNF-induced phosphorylation, ubiquitination, and degradation of IkappaBalpha through the inhibition of activation of IkappaBalpha kinase and of Akt. This led to suppression of the phosphorylation and nuclear translocation of p65 and NF-kappaB-dependent reporter gene expression. Magnolol, a honokiol isomer, was equally active. The expression of NF-kappaB-regulated gene products involved in antiapoptosis (IAP1, IAP2, Bcl-x(L), Bcl-2, cFLIP, TRAF1, and survivin), proliferation (cyclin D1, cyclooxygenase-2, and c-myc), invasion (matrix metalloproteinase-9 and intercellular adhesion molecule-1), and angiogenesis (vascular endothelial growth factor) were also down-regulated by honokiol. Honokiol also down-regulated NF-kappaB activation in in vivo mouse dorsal skin model. Thus, overall, our results indicate that NF-kappaB and NF-kappaB-regulated gene expression inhibited by honokiol enhances apoptosis and suppresses osteoclastogenesis and invasion.},
author = {Ahn, K. S.},
doi = {10.1158/1541-7786.MCR-06-0076},
issn = {1541-7786},
journal = {Molecular Cancer Research},
keywords = {Animals,Apoptosis,Apoptosis: drug effects,Biphenyl Compounds,Biphenyl Compounds: pharmacology,Carrier Proteins,Carrier Proteins: antagonists \& inhibitors,Carrier Proteins: metabolism,Cyclin D1,Cyclin D1: antagonists \& inhibitors,Cyclin D1: biosynthesis,Cyclooxygenase 2,Cyclooxygenase 2: genetics,Dose-Response Relationship, Drug,Drug Synergism,Genes, myc,Humans,I-kappa B Proteins,I-kappa B Proteins: metabolism,Lignans,Lignans: pharmacology,Matrix Metalloproteinase 9,Matrix Metalloproteinase 9: biosynthesis,Membrane Glycoproteins,Membrane Glycoproteins: antagonists \& inhibitors,Membrane Glycoproteins: metabolism,Membrane Proteins,Membrane Proteins: genetics,Mice,Molecular Structure,NF-kappa B,NF-kappa B: antagonists \& inhibitors,NF-kappa B: metabolism,Osteoclasts,Osteoclasts: cytology,Osteoclasts: drug effects,Osteogenesis,Osteogenesis: drug effects,Phosphorylation,Phosphorylation: drug effects,Promoter Regions, Genetic,RANK Ligand,Receptor Activator of Nuclear Factor-kappa B,Synaptotagmin I,Synaptotagmin I: metabolism,Tumor Necrosis Factor-alpha,Tumor Necrosis Factor-alpha: antagonists \& inhibit,Tumor Necrosis Factor-alpha: pharmacology,Vascular Endothelial Growth Factor A,Vascular Endothelial Growth Factor A: biosynthesis},
mendeley-groups = {magnolia},
month = sep,
number = {9},
pages = {621--633},
pmid = {16966432},
title = {{Honokiol Potentiates Apoptosis, Suppresses Osteoclastogenesis, and Inhibits Invasion through Modulation of Nuclear Factor- B Activation Pathway}},
url = {http://www.ncbi.nlm.nih.gov/pubmed/16966432},
volume = {4},
year = {2006}
}
</bibtex>

[9]
<bibtex>
@article{Sy2008,
abstract = {The effect of honokiol, an active component of Magnolia officinalis, on glutamate release from isolated nerve terminals (synaptosomes) was examined. Honokiol potently inhibited 4-aminopyridine (4-AP)-evoked glutamate release in a concentration-dependent manner, and this effect resulted from a reduction of vesicular exocytosis and not from an inhibition of Ca(2+)-independent efflux via glutamate transporter. The inhibitory action of honokiol was not due to decreasing synaptosomal excitability or directly interfering with the release process at some point subsequent to Ca(2+) influx, because honokiol did not alter the 4-AP-evoked depolarization of the synaptosomal plasma membrane potential or Ca(2+) ionophore ionomycin-induced glutamate release. Rather, examination of the effect of honokiol on cytosolic [Ca(2+)] revealed that the diminution of glutamate release could be attributed to a reduction in voltage-dependent Ca(2+) influx. Consistent with this, the honokiol-mediated inhibition of 4-AP-evoked glutamate release was completely prevented in synaptosomes pretreated with a wide-spectrum blocker of N-, P-, and Q-type Ca(2+) channels, omega-conotoxin MVIIC. In addition, honokiol modulation of 4-AP-evoked glutamate release appeared to involve a protein kinase C (PKC) signaling cascade, in so far as pretreatment of synaptosomes with the PKC inhibitors Ro318220 or GF109203X all effectively occluded the inhibitory effect of honokiol. Furthermore, honokiol attenuated 4-AP-induced phosphorylation of PKC. Together, these results suggest that honokiol effects a decrease in PKC activation, which subsequently attenuates the Ca(2+) entry through voltage-dependent N- and P/Q-type Ca(2+) channels to cause a decrease in evoked glutamate exocytosis. These actions of honokiol may contribute to its neuroprotective effect in excitotoxic injury.},
author = {Sy, Hiu-Ngar and Wu, Shey-Lin and Wang, Wang-Fu and Wang, Su-Jane},
doi = {10.1002/syn.20568},
issn = {1098-2396},
journal = {Synapse (New York, N.Y.)},
keywords = {Animals,Biphenyl Compounds,Biphenyl Compounds: pharmacology,Cerebral Cortex,Cerebral Cortex: drug effects,Cerebral Cortex: secretion,Dose-Response Relationship, Drug,Glutamic Acid,Glutamic Acid: secretion,Lignans,Lignans: pharmacology,Male,Neural Inhibition,Neural Inhibition: drug effects,Neural Inhibition: physiology,Presynaptic Terminals,Presynaptic Terminals: drug effects,Presynaptic Terminals: secretion,Rats,Rats, Sprague-Dawley,Synaptosomes,Synaptosomes: drug effects,Synaptosomes: secretion},
mendeley-groups = {magnolia},
month = dec,
number = {12},
pages = {890--901},
pmid = {18792989},
title = {{Mechanisms underlying the honokiol inhibition of evoked glutamate release from glutamatergic nerve terminals of the rat cerebral cortex.}},
url = {http://www.ncbi.nlm.nih.gov/pubmed/18792989},
volume = {62},
year = {2008}
}
</bibtex>

[[Category:Supplement data pages]]
[[Category:Anti-inflammatory supplements]]