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| Baicalin is a flavone glycoside, it is a flavonoid. It is the glucuronide of baicalein.
Baicalin is a flavonoid glycoside derived from plants in the genus Scutellaria. It has anxiolytic, anti-cancer and anti-viral properties, and is used in traditional Chinese medicine. Baicalein and baicalin are chemically related, with baicalin being essentially a conjugated (sugar-attached) form of baicalein. This conjugation can modify their biological functions and impacts, making them distinct in certain aspects even though they share several pharmacological properties. baicalin is often hydrolyzed by gut β-glucuronidase to baicalein (aglycone) and then extensively converted to phase-II conjugates (glucuronides/sulfates), which constrains systemic “free” levels after oral dosing. In cancer models, baicalin/baicalein are reported to modulate NF-κB, PI3K/AKT/mTOR, MAPK, and related programs, with downstream effects on cell-cycle arrest, apoptosis, invasion/EMT, and angiogenesis (model-dependent). Baicalein appears to be antioxidant in normal cells (low Cu). In vitro, baicalein can participate in copper-dependent redox cycling under high Cu conditions, leading to ROS generation. Whether this mechanism contributes meaningfully in vivo remains model-dependent. (higher Cu levels) (May applies to other plant polyphenols as well: Ex apigenin, luteolin, EGCG, and resveratrol). Pathways: Apoptosis Pathways (Intrinsic/Mitochondrial): NF-κB Inhibition : PI3K/Akt/mTOR Signaling Pathway downregulate : MAPK/ERK and JNK Signaling Pathways: STAT3 Signaling: (inhibit) Wnt/β-Catenin Signaling Pathway: (suppress) Other Pathways and Effects: • Cell Cycle Arrests (commonly G0/G1 or G2/M) • Anti-angiogenic Effects: By inhibiting VEGF • Modulation of Oxidative Stress: Balancing reactive oxygen species (ROS) levels in cancer cells can also contribute to its antitumor effects. • In normal cells or under conditions of oxidative stress, baicalin has been shown to act as an antioxidant. • In cancer cells, baicalin may increase ROS levels, triggering apoptosis. Lower doses of baicalin might favor antioxidant responses, whereas higher concentrations could lead to ROS accumulation in cancer cells. Redox effects are concentration- and context-dependent; antioxidant behavior predominates in non-tumor oxidative stress models, whereas ROS increases have been reported in some tumor systems at higher concentrations. • If copper levels are elevated in a cancer cell, the additional ROS generated via copper-mediated reactions may synergize with baicalin’s pro-oxidant effects (if observed at higher doses) to exceed the threshold for cancer cell survival. • Conversely, in normal cells with tightly regulated copper levels, baicalin’s antioxidant properties may help in quenching excess ROS or maintaining redox balance. -IC50 in cancer cell lines: Approximately 50–200 µM (with some variability depending on the cell type). • IC50 in normal cell lines: Generally higher, often exceeding 200 µM, though values will vary with experimental conditions. Many in-vitro IC50 values exceed achievable systemic concentrations after oral dosing without advanced formulation. Low oral bioavailability: classic rat PK reports very low absolute BA bioavailability and evidence of enterohepatic cycling
Time-Scale Flag (TSF): P / R / G
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| Cytochrome c ** The term "release of cytochrome c" ** an increase in level for the cytosol. Small hemeprotein found loosely associated with the inner membrane of the mitochondrion where it plays a critical role in cellular respiration. Cytochrome c is highly water-soluble, unlike other cytochromes. It is capable of undergoing oxidation and reduction as its iron atom converts between the ferrous and ferric forms, but does not bind oxygen. It also plays a major role in cell apoptosis. The term "release of cytochrome c" refers to a critical step in the process of programmed cell death, also known as apoptosis. In its new location—the cytosol—cytochrome c participates in the apoptotic signaling pathway by helping to form the apoptosome, which activates caspases that execute cell death. Cytochrome c is a small protein normally located in the mitochondrial intermembrane space. Its primary role in healthy cells is to participate in the electron transport chain, a process that helps produce energy (ATP) through oxidative phosphorylation. Mitochondrial outer membrane permeability leads to the release of cytochrome c from the mitochondria into the cytosol. The release of cytochrome c is a pivotal event in apoptosis where cytochrome c moves from the mitochondria to the cytosol, initiating a chain reaction that leads to programmed cell death. On the one hand, cytochrome c can promote cancer cell survival and proliferation by regulating the activity of various signaling pathways, such as the PI3K/AKT pathway. This can lead to increased cell growth and resistance to apoptosis, which are hallmarks of cancer. On the other hand, cytochrome c can also induce apoptosis in cancer cells by interacting with other proteins, such as Apaf-1 and caspase-9. This can lead to the activation of the intrinsic apoptotic pathway, which can result in the death of cancer cells. Overexpressed in Breast, Lung, Colon, and Prostrate. Underexpressed in Ovarian, and Pancreatic. |
| - | in-vitro, | CRC, | HCT116 | - | in-vitro, | CRC, | LoVo | - | in-vivo, | CRC, | HCT116 |
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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