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| Chrysin is found in passion flower and honey. It is a flavonoid. -To reach plasma levels that might more closely match the concentrations used in in vitro studies (typically micromolar), considerably high doses or advanced delivery mechanisms would be necessary. Chrysin is widely summarized as modulating PI3K/Akt and MAPK pathways in cancer. Chrysin — Chrysin is a naturally occurring flavone-class flavonoid found in honey, propolis, passionflower, and several plants. Its oncology relevance is mainly preclinical: it shows multi-pathway anticancer activity in cell and animal models, but native oral chrysin has very poor systemic bioavailability and no established approved oncology use. Primary mechanisms (ranked):
Bioavailability / PK relevance: Native oral chrysin has very poor systemic exposure because of low aqueous solubility, extensive intestinal/hepatic glucuronidation and sulfation, and efflux; human oral bioavailability has been reported as extremely low, often summarized as below 1%. Formulation strategies such as nanoparticles, lipid systems, micelles, cyclodextrins, or structural analogues are commonly proposed for systemic translation. In-vitro vs systemic exposure relevance: Most anticancer studies use micromolar in-vitro concentrations that are unlikely to be reached in plasma after ordinary oral chrysin. Local intestinal exposure may be more plausible than systemic tumor exposure, but systemic anticancer claims should be treated as formulation-dependent. Clinical evidence status: Preclinical. Evidence is strong enough for mechanistic oncology interest in cell and animal models, including combination/sensitization studies, but there is no mature clinical oncology evidence establishing therapeutic benefit. -Note half-life 2 hrs, BioAv very poor often <1%Pathways: Graphical Pathways - may induce ROS production - ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓ - May Lower AntiOxidant defense in Cancer Cells: NRF2↓, GSH↓ HO1↓ - May Raise AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑, - lowers Inflammation : NF-kB↓, COX2↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓, - inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMP2↓, MMP9↓, TIMP2, uPA↓, VEGF↓, ROCK1↓, FAK↓, RhoA↓, NF-κB↓, ERK↓ - reactivate genes thereby inhibiting cancer cell growth : HDAC↓, P53↑, HSP↓, - cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, CDK4↓, - inhibits Migration/Invasion : TumCMig↓, TumCI↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1↓, - inhibits glycolysis and ATP depletion : HIF-1α↓, cMyc↓, GLUT1↓, LDH↓, HK2↓, PDKs↓, HK2↓, GRP78↑, GlucoseCon↓ - inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, PDGF↓, EGFR↓, - Others: PI3K↓, AKT↓, STAT↓, Wnt↓, AMPK↓, ERK↓, JNK, TrxR, - Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective, - Selectivity: Cancer Cells vs Normal Cells Chrysin Mechanistic Profile
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| Glutathione S-transferases (GSTs) are a family of phase II detoxification enzymes that play key roles in catalyzing the conjugation of glutathione (GSH) to a wide range of electrophilic compounds. This family includes multiple isoenzymes (e.g., GST-α, GST-μ, GST-π) with tissue-specific expression patterns and overlapping as well as distinct substrate specificities. -GSTs are important for detoxifying potentially harmful compounds, including products of oxidative stress, environmental toxins, and chemotherapeutic agents. -They contribute to the cellular defense mechanism against oxidative damage and help maintain cellular redox balance. -Beyond detoxification, GSTs can modulate cell signaling pathways, potentially affecting cell proliferation, apoptosis, and drug resistance. -GST-π is commonly upregulated in several cancers such as breast, lung, colorectal, and hematologic malignancies. -Elevated expression of specific GST isoenzymes—most notably GST-π—has been associated with a poorer prognosis in several cancer types. This is often linked to resistance to chemo- or radiotherapy, as higher GST activity can lead to more efficient detoxification of these agents, reducing their cytotoxic effects. -In contrast, reduced GST expression in some contexts might indicate a less robust detoxification system, which can correlate with increased sensitivity to oxidative stress and possibly a less aggressive tumor phenotype. |
| 2784- | CHr, | Chrysin targets aberrant molecular signatures and pathways in carcinogenesis (Review) |
| - | Review, | Var, | NA |
| 2786- | CHr, | Chemopreventive and therapeutic potential of chrysin in cancer: mechanistic perspectives |
| - | 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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