| Features: polyphenol | |||||||||||||||||||||||||||||||||||||||||||||||||
| Polyphenol of many herbs - rosemary, perilla, sage mint and basil. Rosmarinic acid (RA) is predominantly found in a variety of medicinal and culinary herbs, especially those belonging to the Lamiaceae family, including rosemary (Rosmarinus officinalis), basil (Ocimum basilicum), sage (Salvia officinalis), thyme (Thymus vulgaris), and mints (Mentha spp.). In addition to the Lamiaceae family, RA is also present in plants from other families, such as Boraginaceae and Apiaceae. -Rosmarinic acid is one of the hydroxycinnamic acids, and was initially isolated and purified from the extract of rosemary, a member of mint family (Lamiaceae) -Its chemical structure allows it to act as a free radical scavenger by donating hydrogen atoms to stabilize ROS and free radicals. RA’s dual nature as both a phenolic acid and a flavonoid-related compound enables it to chelate metal ions and prevent the formation of free radicals, thus interrupting oxidative chain reactions. It can modulate the activity of enzymes involved in OS, such as catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), underscoring its potential role in preventing oxidative damage at the cellular level. -divided as rosemary extract, carnosic acid, rosmarinic acid? Summary: -Capacity to chelate transition metal ions, particularly ironChelator (Fe2+) and copper (Cu2+) -RA plus Cu(II)-induced oxidative DNA damage, which causes ROS -rosmarinic acid (RA) as a potential inhibitor of MARK4↓ (inhibiting to tumor growth, invasion, and metastasis) activity (IC50 = 6.204 µM) -Note half-life 1.5–2 hours. BioAv water-soluble, rapid absorbtion Pathways: - varying results of ROS up or down in cancer cells. Plus a report of lowering ROS and no effect on Tumor cell viability. However always seems to lower ROS↓ in normal cells. - ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, - No indication of Lowering AntiOxidant defense in Cancer Cells: - Raises AntiOxidant defense in Normal Cells:(and perhaps even in cancer cells) ROS↓, NRF2↑***, SOD↑, GSH↑, Catalase↑, - lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓ - inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, VEGF↓, ROCK1↓, RhoA↓, NF-κB↓, ERK↓, MARK4↓ - reactivate genes thereby inhibiting cancer cell growth(weak) : HDAC2↓, DNMTs↓weak, P53↑, HSP↓, - cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, - inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, EMT↓, - inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓??, LDHA↓, PFKs↓, GRP78↑, GlucoseCon↓ - inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, EGFR↓, - inhibits Cancer Stem Cells (few references) : CSC↓, Hh↓, GLi1↓, - Others: PI3K↓, AKT↓, STAT↓, AMPK, ERK↓, JNK, - Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective, - Selectivity: Cancer Cells vs Normal Cells
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| The Fenton reaction is a chemical reaction that involves the catalytic decomposition of hydrogen peroxide (H2O2) by iron ions (Fe2+ or Fe3+). This reaction produces highly reactive oxygen species (ROS), including hydroxyl radicals (·OH) and superoxide anions (O2·-). Cancer Progression: Increased oxidative stress from the Fenton reaction can promote cancer cell proliferation, survival, and metastasis. ROS can activate various signaling pathways that support tumor growth and resistance to apoptosis. Therapeutic Target: The Fenton reaction has been explored as a potential therapeutic target. Strategies to manipulate iron levels or enhance the production of ROS in cancer cells are being investigated to selectively induce cell death in tumors. Formula Fe2+ + H2O2 → Fe3+ + HO• + OH− Fe3+ + H2O2 → Fe2+ + HOO• + H+ 2 H2O2 → HO• + HOO• + H2O net reaction – The dysregulation of iron metabolism in certain cancers might serve as a biomarker for targeted treatments that employ Fenton reaction-based strategies. – Researchers are investigating strategies that harness or amplify the Fenton reaction to selectively kill cancer cells. - With more available iron, the Fenton reaction can be enhanced, resulting in increased production of hydroxyl radicals. Which can lead to cancer cell death. See the ROS target for more information |
| 1743- | RosA, | New insights into the competition between antioxidant activities and pro-oxidant risks of rosmarinic acid |
| - | Analysis, | Var, | NA |
| 1744- | RosA, | Therapeutic Applications of Rosmarinic Acid in Cancer-Chemotherapy-Associated Resistance and Toxicity |
| - | Review, | Var, | 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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