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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. 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. Cancer Pathway Table: Cinnamon
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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| 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. |
| 1567- | Cin, | Cinnamon: Mystic powers of a minute ingredient |
| - | Review, | Var, | NA |
| 3890- | Cin, | The Therapeutic Roles of Cinnamaldehyde against Cardiovascular Diseases |
| - | Review, | NA, | NA |
| 4259- | Cin, | The Potential of Cinnamon as Anti-Depressant |
| - | 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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