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| Hibiscus sabdariffa (commonly known as Roselle) It is rich in bioactive components such as polyphenols, anthocyanins, flavonoids, organic acids, and other antioxidants. Hibiscus sabdariffa is rich in antioxidants and bioactive compounds that show potential anti-cancer effects by reducing oxidative stress, inhibiting cell proliferation, inducing apoptosis, and modulating inflammatory pathways.
Hibiscus sabdariffa — commonly known as roselle, is an edible medicinal plant whose calyces and leaves contain anthocyanins, polyphenols, flavonoids, phenolic acids, and organic acids. It is classified as a botanical food/nutraceutical and plant-extract modality rather than a defined anticancer drug. Standard abbreviations include HS and H. sabdariffa. The calyx is the predominant food and beverage source, whereas several anticancer studies have used leaf extracts, anthocyanin-rich fractions, or polyphenol-enriched preparations that are not compositionally equivalent to ordinary hibiscus tea. Important constituents include delphinidin-3-sambubioside, cyanidin-3-sambubioside, protocatechuic acid, and other polyphenols. -Calyx — the thick, fleshy red structure surrounding the base of the flower and later the seed capsule. This is the main material used for hibiscus tea, beverages, extracts, and most commercial supplements. It is especially rich in anthocyanins, organic acids, and polyphenols. Primary mechanisms (ranked):
Bioavailability / PK relevance: Hibiscus anthocyanins are orally absorbed but have low systemic bioavailability and are rapidly metabolized and eliminated. Human pharmacokinetic studies demonstrate circulating anthocyanin-derived compounds after oral Hibiscus extract, but exposure to intact parent anthocyanins is substantially lower than concentrations commonly used in mechanistic cell-culture studies. Extract composition, plant part, cultivar, processing, and extraction method materially affect exposure. In-vitro vs systemic exposure relevance: Many anticancer experiments use approximately hundreds of µg/mL to mg/mL of crude or polyphenol-enriched extract, or high-µM to millimolar concentrations of individual phenolic compounds. These concentrations generally exceed plausible circulating concentrations following ordinary dietary Hibiscus consumption. Direct translation of in-vitro anticancer potency to oral tea or supplement use is therefore poor. Local gastrointestinal exposure may be considerably higher than systemic exposure. Clinical evidence status: Cancer evidence is predominantly preclinical, consisting of cell-culture studies and limited animal models; there is no established human anticancer efficacy and no validated Hibiscus anticancer dosing regimen. Human RCT evidence is considerably stronger for blood-pressure reduction and some cardiometabolic effects than for cancer treatment. Hibiscus should therefore be categorized as preclinical for anticancer therapy, not as an established cancer adjunct. Oral Hibiscus preparations are generally well tolerated in short-term human studies, but clinically relevant hypotensive and glucose-lowering effects can occur, creating potential additive effects with antihypertensive or antidiabetic therapy. Hibiscus sabdariffa Cancer-Relevant Mechanisms
P: 0–30 min R: 30 min–3 hr G: >3 hr |
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| In all eukaryotic cells, intracellular Ca2+ levels are maintained at low resting concentrations (approximately 100 nM) by the activity of the major Ca2+ extrusion system, the plasma membrane Ca2+-ATPase (PMCA), which exchanges extracellular protons (H+) for cytosolic Ca2+. Indeed, sustained elevation of [Ca2+]C in the form of overload, saturating all Ca2+-dependent effectors, prolonged decrease in [Ca2+]ER, causing ER stress response, and high [Ca2+]M, inducing mitochondrial permeability transition (MPT), are considered to be pro-death factors. In cancer the Ca2+-handling toolkit undergoes profound remodelling (figure 1) to favour activation of Ca2+-dependent transcription factors, such as the nuclear factor of activated T cells (NFAT), c-Myc, c-Jun, c-Fos that promote hypertrophic growth via induction of the expression of the G1 and G1/S phase transition cyclins (D and E) and associated cyclin-dependent kinases (CDK4 and CDK2). Thus, cancer cells may evade apoptosis through decreasing calcium influx into the cytoplasm. This can be achieved by either downregulation of the expression of plasma membrane Ca2+-permeable ion channels or by reducing the effectiveness of the signalling pathways that activate these channels. Such protective measures would largely diminish the possibility of Ca2+ overload in response to pro-apoptotic stimuli, thereby impairing the effectiveness of mitochondrial and cytoplasmic apoptotic pathways. Voltage-Gated Calcium Channels (VGCCs): Overexpression of VGCCs has been associated with increased tumor growth and metastasis in various cancers, including breast and prostate cancer. Store-Operated Calcium Entry (SOCE): SOCE mechanisms, such as STIM1 and ORAI1, are often upregulated in cancer cells, contributing to enhanced cell survival and proliferation. High intracellular calcium levels are associated with increased cell proliferation and migration, leading to a poorer prognosis. Calcium signaling can also influence hormone receptor status, affecting treatment responses. Increased Ca²⁺ signaling is associated with advanced disease and metastasis. Patients with higher CaSR expression may have a worse prognosis due to enhanced tumor growth and resistance to apoptosis. -Ca2+ is an important regulator of the electric charge distribution of bio-membranes. |
| 7361- | HibSad, | Hibiscus sabdariffa L. - a phytochemical and pharmacological review |
| - | Review, | Var, | 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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