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| Hyperoside is a chemical compound and a quercetin galactoside. It is found in various plants and has antibacterial, antifungal and UV blocking properties. Hyperoside is an active ingredient in plants, such as Hypericum monogynum in Hypericaceae, Crataegus pinnatifida in Rosaceae and Polygonum aviculare in Polygonaceae. Hyperoside is a natural flavonol glycoside in various plants, such as Crataegus pinnatifida Bge, Forsythia suspensa, and Cuscuta chinensis Lam. **-Note NRF2 up in normal cells and down in cancer cells** -not currently available as supplement, but it is in Hawthorn Extract. (Natural factors lists it as hyperoside equilvalents 6.6mg/300mg) Hyperoside — also known as hyperin and quercetin-3-O-β-D-galactoside, is a naturally occurring flavonol glycoside consisting of quercetin conjugated at the 3-position to β-D-galactose. It is found in numerous medicinal and dietary plants including species of Hypericum, Crataegus, Polygonum, and Rhododendron. It is classified as a plant-derived flavonoid/polyphenolic small molecule. Hyperoside has antioxidant and cytoprotective activity in many normal-cell models but can produce cancer-selective stress responses, apoptosis, autophagy, and ferroptosis depending on tumor type and concentration. Its aglycone is quercetin. Primary mechanisms (ranked):
Bioavailability / PK relevance: Oral bioavailability of intact hyperoside appears poor. Rat studies found very low systemic exposure after intragastric administration, with substantially greater exposure after parenteral administration. Hyperoside is relatively resistant to gastrointestinal hydrolysis compared with isoquercitrin, which may limit absorption of its quercetin aglycone. Distribution studies indicate preferential accumulation in kidney relative to several other organs. Nanoparticle and liposomal formulations have therefore been investigated to improve delivery and tumor or mitochondrial accumulation. Long-term high-dose exposure warrants caution because renal toxicity has been reported preclinically. In-vitro vs systemic exposure relevance: Many anticancer experiments use approximately 10–100 µM hyperoside, while some autophagy studies have used 0.5–2 mM. These concentrations, particularly the millimolar experiments, are unlikely to represent achievable concentrations of unchanged hyperoside following conventional oral administration. Consequently, direct translation of many in-vitro anticancer effects to oral supplementation is weak without an exposure-enhancing formulation. Clinical evidence status: Preclinical. Anticancer activity has been demonstrated in multiple cancer-cell systems and several mouse xenograft or chemically induced tumor models, including lung, breast, pancreatic, skin, liver, colorectal, esophageal, and hematologic malignancy models. There is currently no established human anticancer efficacy, approved oncology indication, or convincing interventional clinical evidence for purified hyperoside. FDA substance registration identifies hyperoside chemically but does not constitute drug approval. Hyperoside Cancer-Relevant Mechanisms
Hyperoside and Alzheimer's disease: Hyperoside has significant preclinical neuroprotective evidence in Alzheimer's disease models. Long-term administration in APP/PS1 transgenic mice improved spatial learning and memory and reduced amyloid plaque deposition, tau phosphorylation, activated microglia and astrocytes, neuroinflammation, and oxidative stress. Mechanistic evidence implicates suppression of BACE1 and GSK-3β, protection of the blood-brain barrier, inhibition of mitochondrial and caspase-dependent apoptosis, and broader antioxidant/anti-inflammatory effects. Evidence remains preclinical; clinical efficacy in human Alzheimer's disease has not been established. Hyperoside Alzheimer's-Relevant Mechanisms
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| Source: CGL-CS |
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| Mitogen-activated protein kinases (MAPKs) are a group of proteins involved in transmitting signals from the cell surface to the nucleus, playing a crucial role in various cellular processes, including growth, differentiation, and apoptosis (programmed cell death). MAPK Pathways: The MAPK family includes several pathways, the most notable being: 1.ERK (Extracellular signal-Regulated Kinase): Often associated with cell proliferation and survival. 2.JNK (c-Jun N-terminal Kinase): Typically involved in stress responses and apoptosis. 3.p38 MAPK: Associated with inflammatory responses and apoptosis. Inhibitors: Targeting the MAPK pathway has become a strategy in cancer therapy. For example, BRAF inhibitors (like vemurafenib) are used in treating melanoma with BRAF mutations. Altered Expression Levels: Overexpression: Many cancers exhibit overexpression of MAPK pathway components, such as RAS, BRAF, and MEK. This overexpression can lead to increased signaling activity, promoting cell proliferation and survival. Downregulation: In some cases, negative regulators of the MAPK pathway (e.g., MAPK phosphatases) may be downregulated, leading to enhanced MAPK signaling. The expression levels of MAPK pathway components can serve as biomarkers for cancer diagnosis, prognosis, and treatment response. For example, high levels of phosphorylated ERK (p-ERK) may indicate active MAPK signaling and poor prognosis in certain cancers. Numerous reports indicate that the MAPK pathway plays a major role in tumor progression and invasion, while inhibition of MAPK signaling reduces invasion. |
| 7565- | HYP, | Potential Implications of Hyperoside on Oxidative Stress-Induced Human Diseases: A Comprehensive Review |
| - | Review, | AD, | NA |
| 7554- | HYP, | Effect of hyperoside on the apoptosis of A549 human non‑small cell lung cancer cells and the underlying mechanism |
| - | in-vitro, | NSCLC, | A549 |
| 7548- | HYP, | Mechanistic evaluation of hyperoside against non-small cell lung cancer: a combined approach of network pharmacology and in vitro experimental validation |
| - | in-vitro, | NSCLC, | A549 |
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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