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(Synonyms: 款冬酮) 目录号 : GC38976

Tussilagone, isolated from the flower of buds of Tussilago farfara (Compositae), is a sesquiterpenoid that is used as a traditional oriental medicine for asthma and bronchitis. It shows anti-inflammatory activity in in vitro studies.

Tussilagone Chemical Structure

Cas No.:104012-37-5

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1mg
¥368.00
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5mg
¥966.00
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10mg
¥1,645.00
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20mg
¥2,800.00
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产品描述

Tussilagone, isolated from the flower of buds of Tussilago farfara (Compositae), is a sesquiterpenoid that is used as a traditional oriental medicine for asthma and bronchitis. It shows anti-inflammatory activity in in vitro studies.

Chemical Properties

Cas No. 104012-37-5 SDF
别名 款冬酮
Canonical SMILES CC/C(C)=C/C(O[C@H]1C([C@]2([H])CC([C@H]([C@H](OC(C)=O)C)[C@@]2([H])[C@H](C(C)C)C1)=O)=C)=O
分子式 C23H34O5 分子量 390.51
溶解度 DMSO: 62.5 mg/mL (160.05 mM) 储存条件 -20°C, protect from light
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1 mM 2.5608 mL 12.8038 mL 25.6075 mL
5 mM 0.5122 mL 2.5608 mL 5.1215 mL
10 mM 0.2561 mL 1.2804 mL 2.5608 mL
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Research Update

Tussilagone Reduces Tumorigenesis by Diminishing Inflammation in Experimental Colitis-Associated Colon Cancer

Biomedicines 2020 Apr 11;8(4):86.PMID:32290483DOI:10.3390/biomedicines8040086.

Background: Tussilagone, a major component of Tussilago farfara L., has anti-angiogenic and anti-inflammatory effects. However, the therapeutic and preventive activity of Tussilagone in colitis-associated colon carcinogenesis is unknown. Methods: We intended to investigate the therapeutic effects and the potential mechanism of action underlying the pharmacological activity of Tussilagone on colitis-associated colon cancer induced in mice using azoxymethane (AOM)/dextran sulfate sodium (DSS). We injected BALB/c mice with AOM and administered 2% DSS in drinking water. The mice were given Tussilagone (2.5 and 5 mg/kg body weight) and colon tissues was collected at 72 days. We used Western blotting, immunohistochemistry and real-time RT-PCR analyses to examine the tumorigenesis and inflammatory status of the colon. Results: Tussilagone administration significantly reduced the formation of colonic tumors. In addition, Tussilagone treatment markedly reduced the inflammatory mediators and increased heme oxygease-1 in protein and mRNA levels in colon tissues. Meanwhile, nuclear NF-κB-positive cells were elevated and nuclear Nrf2-positive cells were demised by Tussilagone treatment in colon tissues. Tussilagone also reduced cell proliferation, induced apoptosis and decreased the β-catenin expression. Conclusions: Tussilagone administration decreases the inflammation and proliferation induced by AOM/DSS and induced apoptosis in colon tissue. Overall, this study indicates the potential value of Tussilagone in suppressing colon tumorigenesis.

Tussilagone promotes osteoclast apoptosis and prevents estrogen deficiency-induced osteoporosis in mice

Biochem Biophys Res Commun 2020 Oct 22;531(4):508-514.PMID:32807498DOI:10.1016/j.bbrc.2020.07.083.

Osteoporosis is a degenerative disease characterized by reduced bone mass, in which deregulated bone remodeling by osteoclasts and osteoblasts is a main pathogenesis. Although recently Tussilagone, a major active component of flower buds of Tussilago farfara, has been shown to inhibit osteoclastogenesis, its effect on estrogen deficiency-induced osteoporosis remains unknown. This study examined the effect of Tussilagone on bone loss in ovariectomized mice and further explored its impact on osteoclast apoptosis and osteoblast formation in addition to osteoclastogenesis. Tussilagone suppression of osteoclastogenesis was confirmed in bone marrow derived macrophages, which was observed with the 1/10 concentration of that of the previous study. As demonstrated by ApoPercentage dye staining and Western blotting, Tussilagone enhanced apoptosis in differentiated osteoclasts by increasing estrogen receptor α and Fas ligand expression. On the contrary, either osteoblast differentiation or mineralization was not affected by Tussilagone. Lastly, administering Tussilagone to mice for 6 weeks prevented trabecular microarchitecture impairment in ovariectomized mice compared to vehicle control groups. These findings suggest that Tussilagone or Tussilago farfara prevents osteoporotic bone loss by suppressing osteoclast differentiation and inducing osteoclast apoptosis, and that it may therefore offer a possible remedy against resorptive bone diseases.

Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice

Int J Mol Sci 2017 Dec 18;18(12):2744.PMID:29258263DOI:10.3390/ijms18122744.

Tussilagone, extracted from Tussilago farfara is an oriental medicine used for asthma and bronchitis. We investigated its mechanism of action, its inhibitory effects on lipopolysaccharide-induced inflammation in macrophages, and its impact on viability in a cecal ligation and puncture (CLP)-induced mouse model of sepsis. Tussilagone suppressed the expression of the inflammatory mediators, nitric oxide and prostaglandin E2, and the inflammatory cytokines, tumor necrosis factor-alpha (TNF-α) and high-mobility group box 1 (HMGB1), in lipopolysaccharide-stimulated RAW 264.7 cells and peritoneal macrophages. Tussilagone also reduced the activation of the mitogen-activated protein kinases and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) involved in the activation of various inflammatory mediators in activated macrophages. Moreover, Tussilagone administration (1 mg/kg and 10 mg/kg) produced decreased mortality and lung injury in CLP-activated septic mice. Augmented expression of cyclooxygenase (COX)-2 and TNF-α in pulmonary alveolar macrophages of septic mice were attenuated by Tussilagone administration. Tussilagone also suppressed the induction of nitric oxide, prostaglandin E2, TNF-α and HMGB1 in the serum of the septic mice. Overall, Tussilagone exhibited protective effects against inflammation and polymicrobial sepsis by suppressing inflammatory mediators possibly via the inhibition of NF-κB activation and the MAP kinase pathway. These results suggest the possible use of Tussilagone for developing novel therapeutic modalities for sepsis and other inflammatory diseases.

Tussilagone protects acute lung injury from PM2.5 via alleviating Hif-1α/NF-κB-mediated inflammatory response

Environ Toxicol 2022 May;37(5):1198-1210.PMID:35112795DOI:10.1002/tox.23476.

Environmental pollution, especially particulate matter in the air, is a serious threat to human health. Long-term inhalation of particulate matter with a diameter < 2.5 μm (PM2.5) induced irreversible respiratory and lung injury. However, it is not clear whether temporary exposure to massive PM2.5 would result in epithelial damage and lung injury. More importantly, it is urgent to clarify the mechanisms of PM2.5 cytotoxicity and develop a defensive and therapeutic approach. In this study, we demonstrated that temporary exposure with PM2.5 induced lung epithelial cell apoptosis via promoting cytokines expression and inflammatory factors secretion. The cytotoxicity of PM2.5 could be alleviated by Tussilagone (TSL), which is a natural compound isolated from the flower buds of Tussilago farfara. The mechanism study indicated that PM2.5 promoted the protein level of Hif-1α by reducing its degradation mediated by PHD2 binding, which furtherly activated NF-κB signaling and inflammatory response. Meanwhile, TSL administration facilitated the interaction of the Hif-1α/PHD2 complex and restored the Hif-1α protein level increased by PM2.5. When PHD2 was inhibited in epithelial cells, the protective function of TSL on PM2.5 cytotoxicity was attenuated and the expression of cytokines was retrieved. Expectedly, the in vivo study also suggested that temporary PM2.5 exposure led to acute lung injury. TSL treatment could effectively relieve the damage and decrease the expression of inflammatory cytokines by repressing Hif-1α level and NF-κB activation. Our findings provide a new therapeutic strategy for air pollution-related respiratory diseases, and TSL would be a potential preventive medicine for PM2.5 cytotoxicity.

Tussilagone Suppresses Angiogenesis by Inhibiting the VEGFR2 Signaling Pathway

Front Pharmacol 2019 Jul 5;10:764.PMID:31333473DOI:10.3389/fphar.2019.00764.

Tussilagone (TSL) is a sesquiterpenoid isolated from Tussilago farfara, which has been used as a traditional medicine for the treatment of asthma and bronchitis. It also takes part in the anti-inflammatory and antioxidant effects, but its role in angiogenesis is unknown. Angiogenesis is a cancer feature that is essential for supplying oxygen and nutrients to all proliferating tumor cells. Here, we demonstrated that TSL significantly inhibited the proliferation, migration, invasion, and tube formation of primary human umbilical vascular endothelial cell (HUVEC) in vitro. Also, TSL inhibited vascular endothelial growth factor (VEGF)-induced angiogenesis revealed by Matrigel plug assay in vivo. At present, we observed that TSL inhibited the activity of VEGFR2 signal pathway induced by VEGF. These findings suggested that TSL may serve as a potential therapeutic target in the angiogenesis.