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tussilago japonica/anticancerigen
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Modification of the Myelotoxic and Antitumor Effects of Polychemotherapy by Polysaccharides from Tussilago farfara L.
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The experiments on C57Bl/6 mice with Lewis lung carcinoma showed that addition of Tussilago farfara L. polysaccharides to conventional cisplatin/paclitaxel polychemotherapy moderated neutropenia caused by antitumor therapy and increased its efficiency. The stimulating effect of polysaccharides on
Sesquiterpenoids from Tussilago farfara Flower Bud Extract for the Eco-Friendly Synthesis of Silver and Gold Nanoparticles Possessing Antibacterial and Anticancer Activities.
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Sesquiterpenoids from the flower bud extract of Tussilago farfara were effectively utilized as a reducing agent for eco-friendly synthesis of silver and gold nanoparticles. The silver and gold nanoparticles had a characteristic surface plasmon resonance at 416 nm and 538 nm, respectively.
Vibrational spectroscopy and electrophoresis as a "golden means" in monitoring of polysaccharides in medical plant and gels.
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In recent years, some bioactive polysaccharides isolated from natural sources have attracted much attention in the field of biochemistry and pharmacology. Of them, polysaccharides or their glycoconjugates were shown to exhibit multiple biological activities including anticarcinogenic, anticoagulant,
Tussilago farfara L. augments TRAIL-induced apoptosis through MKK7/JNK activation by inhibition of MKK7‑TIPRL in human hepatocellular carcinoma cells.
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Induction of apoptosis through activation of the TRAIL pathway is considered to be a promising anticancer strategy due to its ability to selectively induce apoptosis in cancer cells. However, the ability of cancer cells to acquire TRAIL resistance has limited the clinical translation of this
Effects of Tussilago farfara L. Polysaccharides on the Expression of PD-1 (CD279) and PD-L1 (CD274) in Peripheral Blood and Tumor Tissue Lymphocytes in Mice with Lewis Lung Carcinoma
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One of prospective methods for immunotherapy of tumors is modulation via immunological checkpoints, specifically, via the PD-1(CD279)/PD-L1(CD274) system. Interactions between tumor cell receptor (CD279) and the ligand on lymphocytes (CD274) leads to lymphocyte inactivation, which allows tumor
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