Magnolia bark extract
Information on nutritional supplements people with ALS have been taking
Effects on ALS
Magnolia is a PPAR-gamma activator and GABA-alpha receptor agonist. [source needed]
Studies using human U937 promonocytes cells suggested that magnolol, a low molecular weight lignan isolated from Magnolia officinalis, differentially down-regulated the pharmacologically induced expression of NF-kappaB-regulated inflammatory gene products MMP-9, IL-8, MCP-1, MIP-1alpha, TNF-alpha. [1]
Discussion threads on the ALSTDI forum
References
[1] <bibtex> @article{Tse2007, abstract = {The mis-regulation of nuclear factor-kappa B (NF-kappaB) signal pathway is involved in a variety of inflammatory diseases that leds to the production of inflammatory mediators. Our studies using human U937 promonocytes cells suggested that magnolol, a low molecular weight lignan isolated from the medicinal plant Magnolia officinalis, differentially down-regulated the pharmacologically induced expression of NF-kappaB-regulated inflammatory gene products MMP-9, IL-8, MCP-1, MIP-1alpha, TNF-alpha. Pre-treatment of magnolol blocked TNF-alpha-induced NF-kappaB activation in different cell types as evidenced by EMSA. Magnolol did not directly affect the binding of p65/p50 heterodimer to DNA. Immunoblot analysis demonstrated that magnolol inhibited the TNF-alpha-stimulated phosphorylation and degradation of the cytosolic NF-kappaB inhibitor IkappaBalpha and the effects were dose-dependent. Mechanistically, a non-radioactive IkappaB kinases (IKK) assay using immunoprecipitated IKKs protein demonstrated that magnolol inhibited both intrinsic and TNF-alpha-stimulated IKK activity, thus suggesting a critical role of magnolol in abrogating the phosphorylation and degradation of IkappaBalpha. The involvement of IKK was further verified in a HeLa cell NF-kappaB-dependent luciferase reporter system. In this system magnolol suppressed luciferase expression stimulated by TNF-alpha and by the transient transfection and expression of NIK (NF-kappaB-inducing kinase), wild type IKKbeta, constitutively active IKKalpha and IKKbeta, or the p65 subunit. Magnolol was also found to inhibit the nuclear translocation and phosphorylation of p65 subunit of NF-kappaB. In line with the observation that NF-kappaB activation may up-regulate anti-apoptotic genes, it was shown in U937 cells that magnolol enhanced TNF-alpha-induced apoptotic cell death. Our results suggest that magnolol or its derivatives may have potential anti-inflammatory actions through IKK inactivation.}, author = {Tse, Anfernee Kai-Wing and Wan, Chi-Keung and Zhu, Guo-Yuan and Shen, Xiao-Ling and Cheung, Hon-Yeung and Yang, Mengsu and Fong, Wang-Fun}, doi = {10.1016/j.molimm.2006.12.004}, issn = {0161-5890}, journal = {Molecular immunology}, keywords = {Anti-Inflammatory Agents, Non-Steroidal,Anti-Inflammatory Agents, Non-Steroidal: pharmacol,Apoptosis,Apoptosis: drug effects,Biphenyl Compounds,Biphenyl Compounds: pharmacology,Cell Line, Tumor,Cytokines,Cytokines: genetics,Dimerization,Down-Regulation,Gene Expression Regulation,Gene Expression Regulation: drug effects,Humans,I-kappa B Kinase,I-kappa B Kinase: antagonists \& inhibitors,I-kappa B Kinase: metabolism,Lignans,Lignans: pharmacology,Lipopolysaccharides,Lipopolysaccharides: pharmacology,Matrix Metalloproteinase 9,Matrix Metalloproteinase 9: genetics,NF-kappa B,NF-kappa B p50 Subunit,NF-kappa B p50 Subunit: antagonists \& inhibitors,NF-kappa B p50 Subunit: metabolism,NF-kappa B: drug effects,NF-kappa B: metabolism,Phosphorylation,Phosphorylation: drug effects,Transcription Factor RelA,Transcription Factor RelA: antagonists \& inhibitor,Transcription Factor RelA: metabolism,Tumor Necrosis Factor-alpha,Tumor Necrosis Factor-alpha: genetics,Tumor Necrosis Factor-alpha: pharmacology}, mendeley-groups = {magnolia}, month = apr, number = {10}, pages = {2647--58}, pmid = {17240450}, title = Template:Magnolol suppresses NF-kappaB activation and NF-kappaB regulated gene expression through inhibition of IkappaB kinase activation., url = {http://www.ncbi.nlm.nih.gov/pubmed/17240450}, volume = {44}, year = {2007} } </bibtex>
