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| Brazilian Green Propolis often considered best • Derived from Baccharis dracunulifolia, this type is rich in artepillin C. • It has been widely researched for its anticancer, anti-inflammatory, and antioxidant properties. -Propolis common researched flavonoids :chrysin, pinocembrin, galangin, pinobanksin(Pinocembrin) -most representative phenolic acids were caffeic acid, p-coumaric acid, and ferulic acid, as well as their derivatives, DMCA and caffeic acid prenyl, benzyl, phenylethyl (CAPE), and cinnamyl esters -One of the most studied active compounds of a poplar-type propolis is caffeic acid phenethyl ester (CAPE) -caffeic acid phenethyl ester (CAPE), galangin, chrysin, nemorosone, propolin G, artepillin C, cardanol, pinocembrin, pinobanksin, chicoric acid, and phenolic acids (caffeic acid, ferulic acid, and coumaric acid), as well as luteolin, apigenin, myricetin, naringenin, kaempferol, quercetin, polysaccharides, tannins, terpenes, sterols, and aldehydes -content highly variable based on location and extraction Two main factors of interest: 1. affects interstitual fluild pH 2. high concentration raises ROS (Reactive Oxygen Species), while low concentration may reduce ROS - Artepillin-C (major phenolic compounds found in Brazilian green propolis (BGP)) - caffeic acid major source Propolis is chemically diverse (300+ compounds reported) and composition depends on botanical/geographic source. Antibacterial activity is documented in classic literature (often stronger against Gram+). CAPE from propolis has reported preferential tumor cytotoxicity in early landmark work (often cited in antimicrobial paper references) Do not combine with 2DG Pathways: -Propolis compounds (e.g., artepillin C, caffeic acid phenethyl ester [CAPE]) can trigger apoptosis (programmed cell death) in cancer cells. -Propolis has been shown to inhibit NF‑κB activation. -Propolis extracts can cause cell cycle arrest at specific checkpoints (e.g., G0/G1 or G2/M phases). -Enhance the body’s antitumor immune responses, for example by activating natural killer (NK) cells and modulating cytokine profiles. -Note half-life no standard, high variablity of content. BioAv poor water solubility, and low oral bioavailability. Pathways: - high concentration may induce ROS production, while low concentrations mya low it. This may apply to both normal and cancer cells. Normal Cells Example. (Also not sure if high level are acheivable in vivo due to bioavailability) - ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx, SOD↓, GSH↓ Catalase↓ HO1↓ GPx↓ --> - Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑, - lowers Inflammation : NF-kB↓, COX2↓, Pro-Inflammatory Cytokines : NLRP3↓, TNF-α↓, IL-6↓, IL-8↓ - inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, ROCK1↓, FAK↓, RhoA↓, NF-κB↓, TGF-β↓, α-SMA↓, ERK↓ - reactivate genes thereby inhibiting cancer cell growth : HDAC↓, P53↑, - cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓, - inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1, - inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, GRP78↑, GlucoseCon↓ - inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, - Others: PI3K↓, AKT↓, STAT↓, β-catenin↓, AMPK, ERK↓, JNK, - Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective, - Selectivity: Cancer Cells vs Normal Cells
Time-Scale Flag (TSF): P / R / G
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| Hyperglycemia is defined as elevated blood glucose levels and may result from diabetes mellitus, insulin resistance, or stress-induced metabolic changes. – Elevated glucose levels provide abundant energy resources, potentially facilitating rapid tumor cell division and growth. – Some cancers upregulate glucose transporters (such as GLUT1) to utilize the increased availability of glucose. Oxidative Stress and DNA Damage: – Hyperglycemia is associated with the production of reactive oxygen species (ROS) and advanced glycation end-products (AGEs). – Both ROS and AGEs can lead to DNA damage, genomic instability, and alterations in cell signaling pathways that promote tumor progression. – Studies have linked hyperglycemia with increased tumor aggressiveness in several cancer types, including breast, colorectal, and pancreatic cancers. – Patients with hyperglycemia may experience more rapid disease progression and a higher likelihood of metastasis. – In some cases, elevated glucose levels have been associated with chemotherapy resistance and decreased sensitivity to radiation therapy. – Effective control of blood sugar through dietary interventions, medications (e.g., insulin, metformin), and lifestyle modifications may beneficially impact cancer outcomes. – Regular monitoring of blood glucose and hemoglobin A1c (HbA1c) can inform oncologists about potential metabolic challenges during cancer treatment. |
| 1681- | PBG, | Propolis: Its Role and Efficacy in Human Health and Diseases |
| - | 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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