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| Flavonoid glycoside. Responsible for the bitterness of grapefruit. Naringin is a flavonoid glycoside predominantly found in citrus fruits such as grapefruit and oranges. It is known for its antioxidant, anti-inflammatory, and potential anticancer properties. It is hydrolyzed in vivo to naringenin, which exhibits antioxidant and anti-inflammatory activities and modulates signaling pathways (e.g., Nrf2 and NF-κB). In preclinical cancer models, naringin/naringenin is associated with cell-cycle arrest, apoptosis, and reduced invasion/metastasis, often linked to upstream modulation of survival pathways (PI3K/AKT) and stress MAPKs. Oral systemic exposure is limited due to metabolism and conjugation. -Antioxidant Activity -Induction of Apoptosis -Cell Cycle Arrest (often G1 or G2/M) -Anti-inflammatory Effects -**a natural bioenhancer(effects vary) and reported to enhance the bioavailability of drugs by inhibiting cytochrome P450 (CYP3A4 especially grape fruit juice) and P-glycoprotein (P-gp). Naringin/naringenin can inhibit CYP3A4 and P-glycoprotein, contributing to grapefruit–drug interactions and potentially increasing exposure of certain medications. -Usually paired with other bioflavonoids such as quercetin, hesperidin and rutin. -Mainly obtained from grapefruit -Including enhanced solubility, improved bioavailability and targeted delivery. -Antioxidant -Inhibition of CYP19(weak/modest). Naringin suppresses the PI3K/AKT signalling pathway -Wnt/β-catenin, PI3K/Akt, NF-ĸB, and TGF-β pathways -Up-regulation of adenosine monophosphate-activated protein kinase (AMPK), and inhibition of gluconeogenesis -Antioxidant effects, by modulating reactive oxygen species (ROS) levels and increasing superoxide dismutase (SOD) -Naringenin can reduce carcinogenesis through pleiotropic processes such as antioxidative, apoptotic-inducing ROS generation, and cell cycle arrest -Revealed new mechanisms underlying the hypolipidemic effects of naringin and naringenin, including regulation of lipid digestion, reverse cholesterol transport, and low-density lipoprotein receptor expression -Low bioavailability (approximately 8.8%) when administered orally. Bioavailability: citrus flavonoid glycosides are hydrolyzed in the gut; systemic plasma levels are often much lower than in vitro MICs.
Time-Scale Flag (TSF): P / R / G
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| Source: CGL-CS |
| Type: oncogene |
| Family of RAS proteins (KRAS, NRAS, and HRAS) have been well described to cause oncogenic transformation. - The expression and mutational status of RAS isoforms are critical in several cancers and are generally linked with a poorer prognosis when mutated. RAS is one of the most frequently activated oncogenic drivers in human cancer. Mutations lock RAS in its GTP-bound active state, making signaling: -Constitutive -Growth-factor independent -Resistant to normal feedback control Key framing: RAS is a true driver oncogene, not just an amplifier. Core Oncogenic Pathways Downstream of RAS RAS sits at the apex of multiple essential signaling cascades: a. MAPK Pathway (RAF–MEK–ERK) -Drives proliferation -Induces cell-cycle genes (Cyclin D, MYC, FOS/AP-1) -Supports invasion and differentiation blockade b. PI3K–AKT–mTOR -Promotes survival and metabolic reprogramming -Enhances resistance to apoptosis -Supports protein synthesis and growth c. RAL-GDS and Others -Cytoskeletal remodeling -Vesicle trafficking -Metastatic behavior Together, these create a multi-axis growth and survival program. |
| 1807- | NarG, | A Systematic Review of the Preventive and Therapeutic Effects of Naringin Against Human Malignancies |
| - | Review, | NA, | 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#:128 Target#:269 State#:% Dir#:1
wNotes=0 sortOrder:rid,rpid