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| Cinnamon is a spice from inner bark from several tree species. Cinnamon refers primarily to bark extracts from Cinnamomum verum (Ceylon cinnamon) and Cinnamomum cassia. Bioactive constituents include cinnamaldehyde, cinnamic acid derivatives, procyanidins, and polyphenols. In cancer models, cinnamon extracts and cinnamaldehyde are most frequently reported to exert anti-proliferative, pro-apoptotic, anti-inflammatory, and anti-angiogenic effects. Mechanistic themes include suppression of NF-κB and PI3K/AKT signaling, modulation of MAPK pathways, induction of mitochondrial apoptosis, and context-dependent ROS elevation in tumor cells. Some studies report inhibition of HIF-1α and glycolytic signaling, though cinnamon is not a direct enzymatic Warburg inhibitor. Effects vary substantially depending on species (Ceylon vs Cassia), preparation (aqueous vs ethanol extract), and dose. Human oncology data remain limited and largely preclinical. -Cinnamaldehyde (CA), an active compound derived from the natural plant cinnamon. CA is an aromatic aldehyde compound, constituting approximately 65% of cinnamon extract - See also HCA, a derivative of CA Biological activity, cinnamaldehyde from Ceylon cinnamon: Antimicrobial activity: 10-50 μM Antioxidant activity: 10-100 μM Anti-inflammatory activity: 20-50 μM Anticancer activity: 50-100 μM Cardiovascular health: 20-50 μM 5 g of Ceylon cinnamon might contain roughly between 30 mg and 150 mg of cinnamaldehyde, with an approximate mid-range estimate of about 70 mg. Assuming a moderate supplemental intake 50–200 mg of cinnamaldehyde, peak plasma levels might be anticipated in the vicinity of 1–10 μM. Primary mechanisms (ranked):
Bioavailability / PK relevance: Cinnamon is compositionally variable; cinnamaldehyde is lipophilic, rapidly absorbed and metabolized, and systemic exposure after oral intake is likely much lower than many in-vitro anticancer concentrations. Extract formulation, species, dose, food matrix, and first-pass metabolism materially affect exposure. In-vitro vs systemic exposure relevance: Many anticancer studies use extract concentrations or cinnamaldehyde levels that may exceed achievable free systemic exposure after ordinary oral intake. Local gastrointestinal exposure may be more plausible than systemic tumor exposure. Clinical evidence status: Preclinical for oncology. Cinnamon has human RCT/meta-analysis literature mainly in metabolic/inflammatory endpoints, but no established clinical anticancer indication. Translational constraints include variable extract chemistry, cassia coumarin hepatotoxicity risk, CYP/herb-drug interaction potential, and uncertain tumor-achievable exposure. Cinnamon Cancer Mechanism Table
TSF: P = 0–30 min (redox and early signaling effects), R = 30 min–3 hr (acute pathway modulation), G = >3 hr (apoptosis, angiogenesis, phenotype changes). |
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| – Some studies have reported upregulated expression of certain GABA receptor subunits (e.g., GABA_A receptor subunits) in breast tumors. – Increased expression has been associated with enhanced cell proliferation and migration, with some reports linking this to a poorer prognosis. -GABAergic transmission is deficient in anxiety. -Neurons expressing GABAA α1 receptors can mediate sedation, -while those expressing GABAA α2 receptors mediate anxiolytic. -In addition, extra-synaptic GABAA α5 receptors can also regulate the activity of hippocampal pyramidal cells, thereby affecting associative temporal and spatial memory Gamma-aminobutyric acid — Gamma-aminobutyric acid is an endogenous non-protein amino acid, inhibitory neurotransmitter, metabolic intermediate, and signaling ligand commonly abbreviated GABA. As a database target, it represents changes in GABA concentration, synthesis, secretion, uptake, extracellular accumulation, or GABA-shunt utilization rather than modulation of a specific GABA receptor. GABA is synthesized from glutamate by GAD1/GAD67 and GAD2/GAD65, transported by GABA transporters, and metabolized primarily by ABAT/GABA transaminase. In cancer, GABA may be produced by tumor, neural, stromal, or immune cells and can influence proliferation, invasion, mitochondrial metabolism, β-catenin signaling, and antitumor immunity. Its biological direction is strongly tumor-, receptor-, concentration-, and compartment-dependent. Typical cancer modulation: Variable/context-dependent. GABA production, secretion, extracellular accumulation, uptake, or GABA-shunt utilization may be ↑ in tumors that exploit GABA for metabolic adaptation, β-catenin activation, growth, invasion, or immune evasion. GABA signaling may instead suppress proliferation or migration in tumors expressing inhibitory GABA receptor configurations. Normal-cell relevance: GABA generally reduces neuronal excitability through GABA receptor signaling and also regulates pancreatic, immune, gastrointestinal, vascular, and endocrine functions. In Alzheimer’s disease, reduced phasic inhibition and excessive astrocyte-derived tonic GABA may coexist in different circuits; therefore total GABA direction alone may not indicate whether GABAergic function is beneficial or pathological. Target classification: Neurotransmitter; amino-acid metabolite; signaling ligand; tumor-microenvironment mediator; metabolic substrate. |
| 3891- | Cin, | Identification of potential targets of cinnamon for treatment against Alzheimer's disease-related GABAergic synaptic dysfunction using network pharmacology |
| - | Analysis, | AD, | 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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