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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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| Tumor Microenvironment: Cancer cells often thrive in a more acidic environment compared to normal cells. This is partly due to the metabolic processes of cancer cells, which can produce lactic acid and other acidic byproducts. The acidic microenvironment can promote tumor growth and invasion. Many tumors exhibit an acidic microenvironment. This is largely due to the high rate of glycolysis (often referred to as the Warburg effect), even in the presence of oxygen, leading to lactate production. Acidification is thought to promote invasion, metastasis, and resistance to certain chemotherapies. The body maintains a relatively stable pH in the blood (around 7.4). However, the pH of tissues can vary, and tumors can exhibit a lower pH. -Normal tissues have a higher extracellular pH than intracellular pH, in cancer is exactly the opposite. (inversion of the pH gradient). Cancer cells often overexpress proton pumps (such as V-ATPase) and transporters that actively extrude protons (H⁺) to maintain an intracellular pH conducive to their growth. Inhibiting these pumps can lead to intracellular acidification and potentially induce apoptosis or render cancer cells more vulnerable to other treatments. Normal pH levels in the body: Nasal: ~6.3 pH Mouth/saliva: 6.2-7.6 pH Stomach: 1-3 pH Small Intestine: 5.9-6.8 pH Colon/Large Intestine: 6.8-7 pH |
| 1658- | PBG, | Body Fluid pH Balance in Metabolic Health and Possible Benefits of Dietary Alkaline Foods |
| - | Review, | Var, | NA |
| 1671- | PBG, | Importance of pH Homeostasis in Metabolic Health and Diseases: Crucial Role of Membrane Proton Transport |
| - | Review, | Nor, | NA |
| 1659- | PBG, | Improvement of insulin resistance, blood pressure and interstitial pH in early developmental stage of insulin resistance in OLETF rats by intake of propolis extracts |
| - | in-vivo, | 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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:137 Target#:250 State#:% Dir#:%
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