| 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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| Cellular stress response related to the endoplasmic reticulum (ER) stress, which involves protein folding, quality control, and signaling pathways. The unfolded protein response (UPR) is the cells' way of maintaining the balance of protein folding in the endoplasmic reticulum. (UPR) is triggered by the presence of misfolded proteins in the endoplasmic reticulum. The UPR is a cellular stress response activated by the accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER). - It is primarily mediated by three ER-resident sensors: IRE1α, PERK, and ATF6. Cancer cells often experience high levels of protein synthesis, hypoxia, nutrient deprivation, and oxidative stress, all of which can activate the UPR. – Numerous studies have reported that key UPR components (e.g., GRP78/BiP, IRE1α, PERK, CHOP) are overexpressed in various malignancies such as breast, pancreatic, lung, and prostate cancers. Unfolded Protein Response is typically upregulated in cancers and is associated with poorer prognosis due to its role in promoting cell survival, adaptation to stress, and therapeutic resistance. Although the UPR harbors the potential for tumor-suppressive (apoptotic) effects under severe stress conditions, its predominant activation in tumors supports an adaptive, protumorigenic state that facilitates cancer progression. Targeting UPR components and modulating this balance remain promising therapeutic strategies. |
| 3002- | RosA, | Anticancer Effects of Rosemary (Rosmarinus officinalis L.) Extract and Rosemary Extract Polyphenols |
| - | Review, | Var, | NA |
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