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| Psoralidin is a prenylated coumestan isolated primarily from Psoralea corylifolia (Babchi). It is not a classical anticancer drug. Psoralidin generally acts to suppress oncogenic signaling and survival pathways while promoting apoptosis in tumor cells. Reported effects (context-dependent, preclinical): -DOWNREGULATES pro-survival pathways (e.g., NF-κB, STAT3) -UPREGULATES apoptotic signaling (caspase activation) -MODULATES androgen receptor signaling in prostate cancer models -SENSITIZES tumor cells to chemo- and radio-induced stress This positions psoralidin as a biologic modulator, not a driver. Across cancer cell and animal models, psoralidin has been associated with: -Apoptosis induction -Caspase activation -Mitochondrial depolarization -Inflammatory pathway suppression -NF-κB inhibition -STAT3 attenuation -Hormone signaling modulation -Androgen receptor suppression (prostate cancer context) -Oxidative stress interaction -Redox imbalance tipping tumor cells toward death under stress Psoralidin is best described as chemopreventive or chemo-sensitizing, not chemoprotective |
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| LDH is a general term that refers to the enzyme that catalyzes the interconversion of lactate and pyruvate. LDH is a tetrameric enzyme, meaning it is composed of four subunits. LDH refers to the enzyme as a whole, while LDHA specifically refers to the M subunit. Elevated LDHA levels are often associated with poor prognosis and aggressive tumor behavior, similar to elevated LDH levels. leakage of LDH is a well-known indicator of cell membrane integrity and cell viability [35]. LDH leakage results from the breakdown of the plasma membrane and alterations in membrane permeability, and is widely used as a cytotoxicity endpoint. However, it's worth noting that some studies have shown that LDHA is a more specific and sensitive biomarker for cancer than total LDH, as it is more closely associated with the Warburg effect and cancer metabolism. Dysregulated LDH activity contributes significantly to cancer development, promoting the Warburg effect (Chen et al., 2007), which involves increased glucose uptake and lactate production, even in the presence of oxygen, to meet the energy demands of rapidly proliferating cancer cells (Warburg and Minami, 1923; Dai et al., 2016b). LDHA overexpression favors pyruvate to lactate conversion, leading to tumor microenvironment acidification and aiding cancer progression and metastasis. Inhibitors: Flavonoids, a group of polyphenols abundant in fruit, vegetables, and medicinal plants, function as LDH inhibitors.
LDH is used as a clinical biomarker for Synthetic liver function, nutrition
Tier A — Direct LDH Enzyme Inhibitors (Validated Catalytic Inhibition)
Tier B — Indirect LDH-Axis Modulators (Glycolysis / Lactate Reduction Without Confirmed Direct Catalytic Inhibition)
Tier A = Direct catalytic LDH inhibition (enzyme-level validation). |
| 4968- | PSO, | Psoralidin: emerging biological activities of therapeutic benefits and its potential utility in cervical cancer |
| - | in-vitro, | Cerv, | 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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