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| Rauwolfia serpentina - Indian Snakeroot, Sarpagandha Type: Botanical extract / indole alkaloid-containing medicinal plant Active Constituents: Reserpine, ajmaline, ajmalicine, serpentine, rescinnamine, and related indole alkaloids. Function: Rauwolfia serpentina contains pharmacologically active indole alkaloids with effects on monoamine transport, adrenergic signaling, cardiovascular regulation, cell proliferation, apoptosis, and other signaling pathways. Cancer: Experimental evidence suggests anticancer activity for Rauwolfia-derived alkaloids, particularly reserpine, including inhibition of proliferation, induction of apoptosis, and cell-cycle disruption. Evidence for whole Rauwolfia serpentina extract is more limited than for isolated constituents or other Rauwolfia species, so species-specific attribution should be maintained. Rauwolfia serpentina — also called Indian snakeroot or Sarpagandha, is a medicinal plant in the Apocynaceae family whose roots contain pharmacologically active monoterpenoid indole alkaloids, most notably reserpine, along with ajmaline, ajmalicine, serpentine, rescinnamine, and related compounds. It is classified as a botanical medicinal product / indole-alkaloid source; Reserpine is the best-characterized constituent and acts primarily as an essentially irreversible vesicular monoamine transporter inhibitor, especially VMAT2, depleting norepinephrine, dopamine, and serotonin from neuronal and sympathetic storage vesicles. Historically, Rauwolfia preparations and reserpine were used as antihypertensive agents. Cancer evidence is substantially stronger for isolated reserpine than for standardized R. serpentina extracts, and results from other Rauvolfia species should not automatically be attributed to R. serpentina. Primary mechanisms (ranked):
Bioavailability / PK relevance: Reserpine is orally absorbed, widely distributed, crosses the blood-brain barrier and placenta, and accumulates substantially in tissues including adipose tissue. Human pharmacokinetic data indicate biphasic elimination, with an early half-life of approximately 4.5 hours and a terminal phase of approximately 11.3 days; pharmacodynamic effects can therefore persist well beyond plasma exposure. Whole-root preparations have variable alkaloid composition and cannot be assumed pharmacokinetically equivalent to purified reserpine. In-vitro vs systemic exposure relevance: Anticancer findings are predominantly from cell-culture or animal experiments using purified reserpine or extracts whose achievable human tumor exposure is uncertain. Concentrations producing cancer-cell effects should therefore not be assumed achievable or safe with oral R. serpentina. Chronic pharmacological effects may occur at low systemic reserpine exposure because VMAT binding and monoamine depletion are prolonged, but this does not establish clinically relevant anticancer exposure. Clinical evidence status: Hypertension: historical controlled human evidence and established pharmacology. Cancer: preclinical only; no established anticancer clinical efficacy. Human studies of Rauwolfia/reserpine primarily concern hypertension rather than cancer. Major constraints include hypotension, bradycardia, CNS monoamine depletion, depression, Parkinsonian/extrapyramidal effects, gastrointestinal hypersecretion, drug interactions, and prolonged pharmacodynamic action. Reserpine-containing labeling also notes animal tumorigenicity and uncertain historical epidemiologic findings concerning breast cancer, making indiscriminate interpretation of reserpine as an anticancer compound inappropriate. Rauwolfia serpentina Cancer-Relevant Mechanisms
P: 0–30 min R: 30 min–3 hr G: >3 hr |
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| Hypoxia-Inducible-Factor 1A (HIF1A gene, HIF1α, HIF-1α protein product) -Dominantly expressed under hypoxia(low oxygen levels) in solid tumor cells -HIF1A induces the expression of vascular endothelial growth factor (VEGF) -High HIF-1α expression is associated with Poor prognosis -Low HIF-1α expression is associated with Better prognosis -Functionally, HIF-1α is reported to regulate glycolysis, whilst HIF-2α regulates genes associated with lipoprotein metabolism. -Cancer cells produce HIF in response to hypoxia in order to generate more VEGF that promote angiogenesis Key mediators of aerobic glycolysis regulated by HIF-1α. -GLUT-1 → regulation of the flux of glucose into cells. -HK2 → catalysis of the first step of glucose metabolism. -PKM2 → regulation of rate-limiting step of glycolysis. -Phosphorylation of PDH complex by PDK → blockage of OXPHOS and promotion of aerobic glycolysis. -LDH (LDHA): Rapid ATP production, conversion of pyruvate to lactate; HIF-1α Inhibitors: -Curcumin: disruption of signaling pathways that stabilize HIF-1α (ie downregulate). -Resveratrol: downregulate HIF-1α protein accumulation under hypoxic conditions. -EGCG: modulation of upstream signaling pathways, leading to decreased HIF-1α activity. -Emodin: reduce HIF-1α expression. (under hypoxia). -Apigenin: inhibit HIF-1α accumulation. |
| 7378- | RS, | Reserpine inhibits DNA repair, cell proliferation, invasion and induces apoptosis in oral carcinogenesis via modulation of TGF-β signaling |
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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wNotes=0 sortOrder:rid,rpid