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| Urolithins are gut microbiota–derived dibenzopyran-6-one metabolites formed from ellagitannins → ellagic acid. They are the bioactive, systemically relevant forms responsible for most of the anticancer, mitochondrial, and signaling effects attributed to pomegranate and berry consumption. Ellagic acid itself is largely confined to the gut lumen; urolithins are what reach circulation and tissues. Urolithin A (UA), Most studied; mitophagy, anticancer, anti-inflammatory Humans fall into urolithin metabotypes: Metabotype Description Approx. Population A Produces UA (best profile) ~40% B Produces UB ± UA ~25–30% 0 Non-producer ~30% ROS Modulation (Context-Dependent) Cancer cells: -Mild ROS ↑ or redox stress → apoptosis, growth arrest Normal cells: -ROS ↓, improved mitochondrial efficiency This duality is why urolithins are less chemo-antagonistic than classic antioxidants. Anticancer Signaling ↓ PI3K/AKT/mTOR ↓ Wnt/β-catenin ↓ NF-κB, STAT3 Cell-cycle arrest (G1/S) Unlike sulforaphane or NAC, urolithins: -Do not strongly upregulate NRF2 in cancer cells -May normalize NRF2 signaling in normal cellsDirect Urolithin A Supplements: Bypass microbiome dependency Urolithin A–type activity — Cancer vs Normal Cell Effects
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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. |
| 4875- | Uro, | Impact of the Natural Compound Urolithin A on Health, Disease, and Aging |
| - | Review, | AD, | NA | - | Review, | Stroke, | NA | - | Review, | ostP, | NA | - | Review, | IBD, | NA |
| 4877- | Uro, | Urolithin-A Derivative UAS03 Improves Cognitive Deficits and Memory by Activating Nrf2 Pathways to Alleviate Oxidative Stress and Neuroinflammation |
| - | in-vivo, | AD, | NA |
| 4837- | Uro, | Urolithins: The Gut Based Polyphenol Metabolites of Ellagitannins in Cancer Prevention, a Review |
| - | Review, | Var, | NA |
| 4833- | Uro, | Unveiling the potential of Urolithin A in Cancer Therapy: Mechanistic Insights to Future Perspectives of Nanomedicine |
| - | Review, | Var, | NA | - | Review, | AD, | NA | - | Review, | IBD, | 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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:383 Target#:66 State#:% Dir#:1
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