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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.
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| Lipid peroxidation is a chain reaction process in which free radicals (often reactive oxygen species, or ROS) attack lipids containing carbon-carbon double bonds, especially polyunsaturated fatty acids. This attack results in the formation of lipid radicals, peroxides, and subsequent breakdown products. Lipid peroxidation can cause damage to cell membranes, leading to increased permeability and disruption of cellular functions. This damage can initiate a cascade of events that may contribute to carcinogenesis. The byproducts of lipid peroxidation, such as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), can form adducts with DNA, leading to mutations. These mutations can disrupt normal cellular processes and contribute to the development of cancer. Lipid peroxidation damages cell membranes, disrupts cellular functions, and can trigger inflammatory responses. It is a marker of oxidative stress and is implicated in many chronic diseases. Negative Prognostic Indicator: In many cancers, high levels of lipid phosphates, particularly S1P, are associated with poor prognosis, indicating a more aggressive tumor phenotype and potential resistance to therapy. Mixed Evidence: The prognostic significance of lipid phosphates can vary by cancer type, with some studies showing that their expression may not always correlate with adverse outcomes. |
| 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
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