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== Effects on ALS == | == Effects on ALS == | ||
| − | + | Magnolia is a PPAR-gamma activator and GABA-alpha receptor agonist [2]. [source needed] | |
| − | Honokiol | + | 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. [2] |
| − | + | 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 == | |
| − | + | [http://www.alstdi.org/forum/yaf_postst53013_magnolia-officinalis.aspx Magnolia Officinalis] | |
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== References == | == 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 = {{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> | ||
