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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.
Time-Scale Flag (TSF): P / R / G
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| Source: HalifaxProj(inhibit) |
| Type: |
| Cyclooxygenase-2 (COX-2) is an enzyme that plays a critical role in the conversion of arachidonic acid to prostaglandins, which are lipid compounds involved in various physiological processes, including inflammation, pain, and fever. COX-2 is an inducible enzyme, meaning its expression is typically low in normal tissues but can be upregulated in response to inflammatory stimuli, growth factors, and certain oncogenic signals. -Cyclooxygenase-2 (COX-2), the rate-limiting enzyme in prostaglandin biosynthesis, plays a key role in inflammation and circulatory homeostasis. -COX-2 is an inducible enzyme that is upregulated in response to pro-inflammatory signals, including cytokines (e.g., IL-1β, TNF-α) and growth factors. COX-2 is often overexpressed in various tumors, including colorectal, breast, lung, and prostate cancers. The prostaglandins produced by COX-2, particularly prostaglandin E2 (PGE2), have several effects that can facilitate cancer progression: Cell Proliferation: PGE2 can promote the proliferation of cancer cells by activating signaling pathways such as the PI3K/Akt and MAPK pathways. Nonselective NSAIDs, such as aspirin and ibuprofen, inhibit both COX-1 and COX-2. Epidemiological studies have suggested that regular use of NSAIDs may reduce the risk of certain cancers, particularly colorectal cancer. Drugs specifically targeting COX-2, such as celecoxib, have been developed. COX-2 and xanthine oxidase are ROS-producing pro-oxidant enzymes that contribute to inflammation. Elevated COX‑2 levels, often found in inflammatory conditions or certain types of cancers, can contribute to increased production of ROS. |
| 5252- | MAG, | Insights on the Multifunctional Activities of Magnolol |
| - | Review, | Var, | NA |
| 1089- | MAG, | Magnolol potently suppressed lipopolysaccharide-induced iNOS and COX-2 expression via downregulating MAPK and NF-κB signaling pathways |
| - | in-vitro, | AML, | RAW264.7 |
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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