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 [5] and GABA-alpha receptor agonist {{#pmid:10591411|squires1999}}. PPAR-gamma agonists reduce glutamate release [9] and increase its uptake by astrocytes [6], and increase expression and enzymatic activity of catalase [7].

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 [3] and downregulates Klf4 expression in rat spinal cord injury [4].

== 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].

== Discussion threads on the ALSTDI forum ==

*[http://www.alstdi.org/forum/yaf_postst53013_magnolia-officinalis.aspx Magnolia Officinalis]
*esp. http://www.als.net/forum/yaf_postsm371719_Magnolia-officinalis.aspx#371719


== 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 ==


[3]
<bibtex>
@article{Zhai2005,
abstract = {We have found that honokiol [4-allyl-2-(3-allyl-4-hydroxy-phenyl)-phenol] can promote neurite outgrowth and mobilize intracellular Ca2+ store in primary cultured rat cortical neurons. In this study, we examined the effects of honokiol on extracellular signal-regulated kinases (ERK1/2) and Akt, and their possible relationship to neurite outgrowth and Ca2+ mobilization. Honokiol-induced neurite outgrowth in the cultured rat cortical neurons was significantly reduced by PD98059, a mitogen-activated protein kinase kinase (MAPKK, MAPK/ERK kinase MEK, direct upstream of ERK1/2) inhibitor, but not by LY294002, a phosphoinositide 3-kinase (PI3K, upstream of Akt) inhibitor. Honokiol also significantly enhanced the phosphorylation of ERK1/2 in a concentration-dependent manner, whereas the effect of honokiol on Akt phosphorylation was characterized by transient enhancement in 10 min and lasting inhibition after 30 min. The phosphorylation of ERK1/2 enhanced by honokiol was inhibited by PD98059 as well as by KN93, a Ca2+/calmodulin-dependent kinase II (CaMK II) inhibitor. Moreover, the products of the phosphoinositide specific phospholipase C (PLC)-derived inositol 1,4,5-triphosphate (IP3) and 1,2-diacylglycerol (DAG) were measured after honokiol treatment. Together with our previous findings, these results suggest that the signal transduction from PLC, IP3, Ca2+, and CaMK II to ERK1/2 is involved in honokiol-induced neurite outgrowth.},
author = {Zhai, Haifeng and Nakade, Kousuke and Oda, Masataka and Mitsumoto, Yasuhide and Akagi, Masaaki and Sakurai, Jun and Fukuyama, Yoshiyasu},
doi = {10.1016/j.ejphar.2005.04.035},
issn = {00142999},
journal = {European Journal of Pharmacology},
keywords = {Animals,Benzylamines,Benzylamines: pharmacology,Biphenyl Compounds,Biphenyl Compounds: pharmacology,Blotting, Western,Calcium-Calmodulin-Dependent Protein Kinases,Calcium-Calmodulin-Dependent Protein Kinases: anta,Calcium-Calmodulin-Dependent Protein Kinases: meta,Cells, Cultured,Cerebral Cortex,Chromones,Chromones: pharmacology,Diglycerides,Diglycerides: biosynthesis,Dose-Response Relationship, Drug,Drugs, Chinese Herbal,Drugs, Chinese Herbal: pharmacology,Enzyme Activation,Enzyme Activation: drug effects,Female,Fetus,Flavonoids,Flavonoids: pharmacology,Inositol 1,4,5-Trisphosphate,Inositol 1,4,5-Trisphosphate: biosynthesis,Lignans,Lignans: pharmacology,Mitogen-Activated Protein Kinase 1,Mitogen-Activated Protein Kinase 1: antagonists \& ,Mitogen-Activated Protein Kinase 1: metabolism,Mitogen-Activated Protein Kinase 3,Mitogen-Activated Protein Kinase 3: antagonists \& ,Mitogen-Activated Protein Kinase 3: metabolism,Models, Biological,Morpholines,Morpholines: pharmacology,Neurites,Neurites: drug effects,Neurites: physiology,Neurons,Neurons: cytology,Neurons: drug effects,Neurons: metabolism,Phosphatidylinositol 3-Kinases,Phosphatidylinositol 3-Kinases: antagonists \& inhi,Phosphorylation,Phosphorylation: drug effects,Pregnancy,Protein Kinase Inhibitors,Protein Kinase Inhibitors: pharmacology,Rats,Rats, Sprague-Dawley,Sulfonamides,Sulfonamides: pharmacology},
mendeley-groups = {magnolia},
month = jun,
number = {2},
pages = {112--117},
pmid = {15922325},
title = {{Honokiol-induced neurite outgrowth promotion depends on activation of extracellular signal-regulated kinases (ERK1/2)}},
url = {http://www.ncbi.nlm.nih.gov/pubmed/15922325},
volume = {516},
year = {2005}
}
</bibtex>

[4]
<bibtex>
@article{Liu2015,
abstract = {STUDY DESIGN: Randomized experimental study.

OBJECTIVE: To investigate the neuroprotective effect of honokiol (HNK) on rats subjected to traumatic spinal cord injury (SCI) and the molecular mechanisms.

SUMMARY OF BACKGROUND DATA: Inflammation contributes to the secondary injury to the spinal cord. Honokiol has been used as a neuroprotective agent because of its strong antioxidant and anti-inflammatory properties. Kruppel-like factor 4 (Klf4) is a newly identified critical target for the anti-inflammatory effect of HNK. Whether HNK can inhibit inflammatory response in rat model of SCI through mediating the expression of Klf4 has yet to be elucidated.

METHODS: Eighty-four adult female Sprague-Dawley rats were randomly divided into 4 groups as sham, SCI, SCI + Vehicle (0.1\% propylene glycol in saline, intraperitoneally), and SCI + HNK (20 mg/kg, intraperitoneally) groups. The influences of HNK on the proinflammatory cytokines, microglial activation, neutrophil infiltration, histological changes, and improvement in motor function were assessed.

RESULTS: In the SCI group, proinflammatory cytokines, microglial activation, neutrophil infiltration, and Klf4 expression levels were increased compared with the sham group (P < 0.001). HNK intervention downregulated the expression of Klf4, reduced the production of proinflammatory cytokines, inhibited microglial activation, and neutrophil infiltration (P < 0.05). Furthermore, HNK also reduced histopathology and improved functional outcome after traumatic SCI.

CONCLUSION: HNK reduces secondary tissue damage and improves locomotor function recovery after SCI through suppressing inflammatory response, and can be used as a potential therapeutic agent for SCI.

LEVEL OF EVIDENCE: NA.},
author = {Liu, Jia and Zhang, Changmeng and Liu, Zhi and Zhang, Jianzheng and Xiang, Zimin and Sun, Tiansheng},
doi = {10.1097/BRS.0000000000000758},
issn = {1528-1159},
journal = {Spine},
mendeley-groups = {magnolia},
month = mar,
number = {6},
pages = {363--8},
pmid = {25774462},
title = {{Honokiol downregulates Kruppel-like factor 4 expression, attenuates inflammation, and reduces histopathology after spinal cord injury in rats.}},
url = {http://www.ncbi.nlm.nih.gov/pubmed/25774462},
volume = {40},
year = {2015}
}
</bibtex>

[5]
<bibtex>
@article{Atanasov2013,
abstract = {BACKGROUND: Peroxisome proliferator-activated receptor gamma (PPAR$\gamma$) agonists are clinically used to counteract hyperglycemia. However, so far experienced unwanted side effects, such as weight gain, promote the search for new PPAR$\gamma$ activators.

METHODS: We used a combination of in silico, in vitro, cell-based and in vivo models to identify and validate natural products as promising leads for partial novel PPAR$\gamma$ agonists.

RESULTS: The natural product honokiol from the traditional Chinese herbal drug Magnolia bark was in silico predicted to bind into the PPAR$\gamma$ ligand binding pocket as dimer. Honokiol indeed directly bound to purified PPAR$\gamma$ ligand-binding domain (LBD) and acted as partial agonist in a PPAR$\gamma$-mediated luciferase reporter assay. Honokiol was then directly compared to the clinically used full agonist pioglitazone with regard to stimulation of glucose uptake in adipocytes as well as adipogenic differentiation in 3T3-L1 pre-adipocytes and mouse embryonic fibroblasts. While honokiol stimulated basal glucose uptake to a similar extent as pioglitazone, it did not induce adipogenesis in contrast to pioglitazone. In diabetic KKAy mice oral application of honokiol prevented hyperglycemia and suppressed weight gain.

CONCLUSION: We identified honokiol as a partial non-adipogenic PPAR$\gamma$ agonist in vitro which prevented hyperglycemia and weight gain in vivo.

GENERAL SIGNIFICANCE: This observed activity profile suggests honokiol as promising new pharmaceutical lead or dietary supplement to combat metabolic disease, and provides a molecular explanation for the use of Magnolia in traditional medicine.},
author = {Atanasov, Atanas G. and Wang, Jian N. and Gu, Shi P. and Bu, Jing and Kramer, Matthias P. and Baumgartner, Lisa and Fakhrudin, Nanang and Ladurner, Angela and Malainer, Clemens and Vuorinen, Anna and Noha, Stefan M. and Schwaiger, Stefan and Rollinger, Judith M. and Schuster, Daniela and Stuppner, Hermann and Dirsch, Verena M. and Heiss, Elke H.},
doi = {10.1016/j.bbagen.2013.06.021},
issn = {03044165},
journal = {Biochimica et Biophysica Acta (BBA) - General Subjects},
keywords = {3T3-L1 Cells,Adipose Tissue,Adipose Tissue: cytology,Adipose Tissue: drug effects,Animals,Biological Products,Biological Products: isolation \& purification,Biological Products: pharmacology,Biphenyl Compounds,Biphenyl Compounds: isolation \& purification,Biphenyl Compounds: pharmacology,Cell Differentiation,Cell Differentiation: drug effects,Diabetes Mellitus, Experimental,Diabetes Mellitus, Experimental: physiopathology,HEK293 Cells,Humans,Lignans,Lignans: isolation \& purification,Lignans: pharmacology,Mice,Molecular Docking Simulation,PPAR gamma,PPAR gamma: agonists},
mendeley-groups = {magnolia},
month = oct,
number = {10},
pages = {4813--4819},
pmid = {23811337},
title = {{Honokiol: A non-adipogenic PPAR$\gamma$ agonist from nature}},
url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3790966\&tool=pmcentrez\&rendertype=abstract},
volume = {1830},
year = {2013}
}
</bibtex>

[6]
<bibtex>
@article{Romera2007,
abstract = {Excessive levels of extracellular glutamate in the nervous system are excitotoxic and lead to neuronal death. Glutamate transport, mainly by glutamate transporter GLT1/EAAT2, is the only mechanism for maintaining extracellular glutamate concentrations below excitotoxic levels in the central nervous system. We recently showed that neuroprotection after experimental ischemic preconditioning (IPC) involves, at least partly, the upregulation of the GLT1/EAAT2 glutamate transporter in astrocytes, but the mechanisms were unknown. Thus, we decided to explore whether activation of the nuclear receptor peroxisome proliferator-activated receptor (PPAR) gamma, known for its antidiabetic and antiinflammatory properties, is involved in glutamate transport. First, we found that the PPARgamma antagonist T0070907 inhibits both IPC-induced tolerance and reduction of glutamate release after lethal oxygen-glucose deprivation (OGD) (70.1\%+/-3.4\% versus 97.7\%+/-5.2\% of OGD-induced lactate dehydrogenase (LDH) release and 61.8\%+/-5.9\% versus 85.9\%+/-7.9\% of OGD-induced glutamate release in IPC and IPC+T0070907 1 mumol/L, respectively, n=6 to 12, P<0.05), as well as IPC-induced astrocytic GLT-1 overexpression. IPC also caused an increase in nuclear PPARgamma transcriptional activity in neurons and astrocytes (122.1\%+/-8.1\% and 158.6\%+/-22.6\% of control PPARgamma transcriptional activity, n=6, P<0.05). Second, the PPARgamma agonist rosiglitazone increased both GLT-1/EAAT2 mRNA and protein expression and [(3)H]glutamate uptake, and reduced OGD-induced cell death and glutamate release (76.3\%+/-7.9\% and 65.5\%+/-15.1\% of OGD-induced LDH and glutamate release in rosiglitazone 1 mumol/l, respectively, n=6 to 12, P<0.05). Finally, we have identified six putative PPAR response elements (PPREs) in the GLT1/EAAT2 promoter and, consistently, rosiglitazone increased fourfold GLT1/EAAT2 promoter activity. All these data show that the GLT1/EAAT2 glutamate transporter is a target gene of PPARgamma leading to neuroprotection by increasing glutamate uptake.},
author = {Romera, Cristina and Hurtado, Olivia and Mallolas, Judith and Pereira, Marta P and Morales, Jes\'{u}s R and Romera, Alejandro and Serena, Joaqu\'{\i}n and Vivancos, Jos\'{e} and Nombela, Florentino and Lorenzo, Pedro and Lizasoain, Ignacio and Moro, Maria A},
doi = {10.1038/sj.jcbfm.9600438},
issn = {0271-678X},
journal = {Journal of Cerebral Blood Flow \& Metabolism},
keywords = {Animals,Astrocytes,Astrocytes: drug effects,Astrocytes: metabolism,Astrocytes: pathology,Benzamides,Benzamides: pharmacology,Blotting, Western,Brain,Brain: blood supply,Brain: drug effects,Brain: metabolism,Cells, Cultured,Chromatography, High Pressure Liquid,Coculture Techniques,Excitatory Amino Acid Transporter 2,Excitatory Amino Acid Transporter 2: genetics,Excitatory Amino Acid Transporter 2: metabolism,Gene Expression,Glutamic Acid,Glutamic Acid: analysis,Glutamic Acid: metabolism,Hypoglycemic Agents,Hypoglycemic Agents: pharmacology,Infarction, Middle Cerebral Artery,Infarction, Middle Cerebral Artery: metabolism,Infarction, Middle Cerebral Artery: pathology,Ischemic Preconditioning,Male,Neurons,Neurons: drug effects,Neurons: metabolism,Neurons: pathology,PPAR gamma,PPAR gamma: metabolism,Promoter Regions, Genetic,Pyridines,Pyridines: pharmacology,RNA, Messenger,RNA, Messenger: analysis,RNA, Messenger: drug effects,Rats,Rats, Inbred F344,Rats, Wistar,Response Elements,Reverse Transcriptase Polymerase Chain Reaction,Thiazolidinediones,Thiazolidinediones: pharmacology},
mendeley-groups = {magnolia},
month = jan,
number = {7},
pages = {1327--1338},
pmid = {17213861},
title = {{Ischemic preconditioning reveals that GLT1/EAAT2 glutamate transporter is a novel PPAR$\gamma$ target gene involved in neuroprotection}},
url = {http://www.ncbi.nlm.nih.gov/pubmed/17213861},
volume = {27},
year = {2007}
}
</bibtex>

[7]
<bibtex>
@article{Romera2007,
abstract = {Excessive levels of extracellular glutamate in the nervous system are excitotoxic and lead to neuronal death. Glutamate transport, mainly by glutamate transporter GLT1/EAAT2, is the only mechanism for maintaining extracellular glutamate concentrations below excitotoxic levels in the central nervous system. We recently showed that neuroprotection after experimental ischemic preconditioning (IPC) involves, at least partly, the upregulation of the GLT1/EAAT2 glutamate transporter in astrocytes, but the mechanisms were unknown. Thus, we decided to explore whether activation of the nuclear receptor peroxisome proliferator-activated receptor (PPAR) gamma, known for its antidiabetic and antiinflammatory properties, is involved in glutamate transport. First, we found that the PPARgamma antagonist T0070907 inhibits both IPC-induced tolerance and reduction of glutamate release after lethal oxygen-glucose deprivation (OGD) (70.1\%+/-3.4\% versus 97.7\%+/-5.2\% of OGD-induced lactate dehydrogenase (LDH) release and 61.8\%+/-5.9\% versus 85.9\%+/-7.9\% of OGD-induced glutamate release in IPC and IPC+T0070907 1 mumol/L, respectively, n=6 to 12, P<0.05), as well as IPC-induced astrocytic GLT-1 overexpression. IPC also caused an increase in nuclear PPARgamma transcriptional activity in neurons and astrocytes (122.1\%+/-8.1\% and 158.6\%+/-22.6\% of control PPARgamma transcriptional activity, n=6, P<0.05). Second, the PPARgamma agonist rosiglitazone increased both GLT-1/EAAT2 mRNA and protein expression and [(3)H]glutamate uptake, and reduced OGD-induced cell death and glutamate release (76.3\%+/-7.9\% and 65.5\%+/-15.1\% of OGD-induced LDH and glutamate release in rosiglitazone 1 mumol/l, respectively, n=6 to 12, P<0.05). Finally, we have identified six putative PPAR response elements (PPREs) in the GLT1/EAAT2 promoter and, consistently, rosiglitazone increased fourfold GLT1/EAAT2 promoter activity. All these data show that the GLT1/EAAT2 glutamate transporter is a target gene of PPARgamma leading to neuroprotection by increasing glutamate uptake.},
author = {Romera, Cristina and Hurtado, Olivia and Mallolas, Judith and Pereira, Marta P and Morales, Jes\'{u}s R and Romera, Alejandro and Serena, Joaqu\'{\i}n and Vivancos, Jos\'{e} and Nombela, Florentino and Lorenzo, Pedro and Lizasoain, Ignacio and Moro, Maria A},
doi = {10.1038/sj.jcbfm.9600438},
issn = {0271-678X},
journal = {Journal of Cerebral Blood Flow \& Metabolism},
keywords = {Animals,Astrocytes,Astrocytes: drug effects,Astrocytes: metabolism,Astrocytes: pathology,Benzamides,Benzamides: pharmacology,Blotting, Western,Brain,Brain: blood supply,Brain: drug effects,Brain: metabolism,Cells, Cultured,Chromatography, High Pressure Liquid,Coculture Techniques,Excitatory Amino Acid Transporter 2,Excitatory Amino Acid Transporter 2: genetics,Excitatory Amino Acid Transporter 2: metabolism,Gene Expression,Glutamic Acid,Glutamic Acid: analysis,Glutamic Acid: metabolism,Hypoglycemic Agents,Hypoglycemic Agents: pharmacology,Infarction, Middle Cerebral Artery,Infarction, Middle Cerebral Artery: metabolism,Infarction, Middle Cerebral Artery: pathology,Ischemic Preconditioning,Male,Neurons,Neurons: drug effects,Neurons: metabolism,Neurons: pathology,PPAR gamma,PPAR gamma: metabolism,Promoter Regions, Genetic,Pyridines,Pyridines: pharmacology,RNA, Messenger,RNA, Messenger: analysis,RNA, Messenger: drug effects,Rats,Rats, Inbred F344,Rats, Wistar,Response Elements,Reverse Transcriptase Polymerase Chain Reaction,Thiazolidinediones,Thiazolidinediones: pharmacology},
mendeley-groups = {magnolia},
month = jan,
number = {7},
pages = {1327--1338},
pmid = {17213861},
title = {{Ischemic preconditioning reveals that GLT1/EAAT2 glutamate transporter is a novel PPAR$\gamma$ target gene involved in neuroprotection}},
url = {http://www.ncbi.nlm.nih.gov/pubmed/17213861},
volume = {27},
year = {2007}
}
</bibtex>

[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>

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