Fucoxanthin is a pigment (reddish brown color) that is found only in brown algae, and is the same type of pigment called carotenoid that is found in vitamin A and β-carotene. It induces apoptosis (DNA cleavage) of cancer cells by activating caspase-8 and -1 (enzyme) in the body. By binding to RBP and reducing blood RBP concentration to normal levels, fucoxanthin improves insulin sensitivity as well as blood glucose, hemoglobin, and hemoglobin A1c levels.
Fucoxanthin, while in its retinol-bound form, induces apoptosis by activating caspase-1 from caspase-8 via retinol receptor and Fas ligand pathways. Some reports also claim that it stops the cell proliferation cycle. Activated caspase-8 cleaves Bid, promoting the release of cytochrome C from the mitochondria. Cytochrome c then binds and activates Apaf-1. This in turn triggers caspase-9 activation. Activated caspase-9 initiates caspase-3 activation, which then activates CAD to induce DNA cleavage.
Fas ligand is a cytokine that mediates apoptosis via Fas cell surface receptor, and is predominantly expressed in activated T-cells. Cells possess receptors called "Fas antigen" on the cell surface that receives information (pro-apoptotic signals) to induce apoptosis. There is also a signaling molecule called "Fas ligand (FasL; Fas ligand)" that sends information upon binding to this receptor (Fas antigen) and it is known that this molecule promotes apoptosis. The word "ligand" refers to a molecule "that binds." Fas ligand is known to be expressed in activated T-cells.
High affinity to retinol-binding protein
With fucoxanthin and related chloroplasts having high affinity to retinol binding protein (RBP), fucoxanthin preferentially binds to RBP, thereby inhibiting the formation of RBP-transthyretin complex. This improves insulin sensitivity and reduces blood RBP concentration to normal levels. (Improves blood glucose and hemoglobin A1c levels.)
Saruchirureito is a novel substance with a CCK (Cladoshiphon caledoniae kylin)/salicylic acid frame that encompasses one Mg (magnesium) atom. Saruchirureito selectively inhibits COX-2, an enzyme that is produced in excess during inflammation. It decreases PGE2 (a molecule involved in the pain signaling pathway) and reduces pain. In addition, Saruchirureito is involved in the suppression bradykinin production, and is effective against various allergies including atopic dermatitis, as well as autoimmune diseases. It is also effective against rheumatism, osteoarthritis, and even refractory chronic diseases such as asthma. Saruchirureito not only affects PGs, but also suppresses the production of IL (interleukin) -4, -5, -13, and -17 which are factors that exacerbate these refractory chronic diseases. COX-2 is transiently produced in the nucleus by cytokine (especially IL-1 and TNF-α) stimulation, and is expressed in inflammatory cells (such as macrophages, neutrophils, fibroblasts, and synovial cells) by inducible enzymes that reside in the nuclear membrane. Prostaglandins (PGs) have anti-inflammatory, analgesic, and antipyretic properties. In the mechanisms of carcinogenesis, chronic inflammatory reactions develop and PG-E2 (Prostaglandin E2) is associated as a factor that affects inflammation. Saruchirureito selectively inhibits cyclooxygenase (COX-2) that is produced in excess during inflammation without affecting COX-1 (an enzyme that maintains gastrointestinal tract, kidney, and platelet), and suppresses the production of inflammation-mediating PGs (prostaglandins) while also significantly promoting anti-cancer, anti-inflammatory, and basic immunostimulatory actions. In addition, by suppressing the production of PGs, basic immunocompetent cells such as NK cells and killer T-cells are activated. However, it does not have an effect on macrophage type cells. The administration of Saruchireito blocks inflammation by selectively inhibiting COX-2, thereby effectively suppressing the patients' pain.
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