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| Lignan found in bark of some magnolia species. Magnolol (MAG) — a bioactive biphenolic compound from Magnolia officinalis derived from the bark (roots and branches) of Magnolia species such as M. officinalis, M. obovata, and M. grandiflora The two main bioactive compounds isolated from these plants are MAG (5,5ʹ-diallyl-2,2ʹ-dihydroxybiphenyl) and Honokiol (3,5ʹ-diallyl-4,2ʹ-dihydroxybiphenyl) (Fig. 1) which are phenolic regioisomers. In the bark extracts of Magnolia plants, the composition of MAG ranges from 1 to 10%, while Honokiol comprises 1 to 5% Magnolol is a biphenolic neolignan isolated from the bark of Magnolia officinalis. It is structurally related to honokiol and is studied for anti-inflammatory, antioxidant, antimicrobial, and neuroactive effects. In preclinical oncology models, magnolol is reported to modulate NF-κB, STAT3, PI3K/AKT, MAPK, Wnt/β-catenin, and redox pathways, with downstream effects on cell-cycle arrest, apoptosis, invasion/EMT, and angiogenesis. Oral bioavailability is limited and many cytotoxic concentrations reported in vitro are in the tens of µM range, often above typical systemic levels from standard supplementation. major pathways and molecular targets involved in magnolol’s anticancer actions: -Apoptosis: ↑ Bax, ↓ Bcl-2, ↑ cytochrome c, ↑ caspase-9, ↑ caspase-3 -Arrests cell cycle at G0/G1 or G2/M phase:↓ Cyclin D1, CDK4, CDK6, Cyclin B1, CDK1 -Inhibits NF-κB activation: ↓ IκBα, COX-2, TNF-α -Inhibits PI3K, Akt, and mTOR phosphorylation -Suppresses angiogenesis: ↓ Bcl-XL, Mcl-1, VEGF, cyclin D1 -Inhibits β-catenin nuclear translocation -increase ROS production in tumor cells → triggers mitochondrial apoptosis -Magnolol activates Nrf2 in normal cells → upregulates HO-1, NQO1: Protects normal tissue from oxidative stress during chemotherapy or inflammation. Most in-vitro IC50 values fall in the 10–100 µM range, often above typical systemic exposure.
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| Peroxisome proliferator-activated receptor gamma (PPAR-γ) is a type of nuclear receptor that plays a crucial role in regulating various biological processes, including glucose metabolism, lipid metabolism, and inflammation. It is primarily expressed in adipose tissue, but it is also found in other tissues, including the colon, breast, and prostate. PPAR-γ has been shown to have both tumor-suppressive and tumor-promoting effects, depending on the type of cancer and the context. In some cancers, activation of PPAR-γ can inhibit cell proliferation and induce apoptosis, while in others, it may promote tumor growth. PPARγ – Plays a central role in adipogenesis, lipid storage, and insulin sensitivity. – Widely expressed in adipose tissue, but also present in colon, breast, and immune cells. – In addition to metabolic functions, PPARγ regulates cell differentiation, apoptosis, and has anti-inflammatory effects. – Ligand binding (such as endogenous fatty acids or synthetic agonists like thiazolidinediones) alters transcriptional programs impacting cell cycle and survival. – In many cases, PPARγ is expressed in tumor cells, and its activation has been linked to induction of differentiation and growth arrest. – However, expression levels can differ based on tumor subtype, with some studies reporting elevated levels while others note reductions in aggressive tumors. – Crosstalk with other signaling pathways (e.g., Wnt/β-catenin, MAPK) can alter PPARγ's net effect in cancer cells. |
| 4528- | MAG, | Pharmacology, Toxicity, Bioavailability, and Formulation of Magnolol: An Update |
| - | Review, | Nor, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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