This product is isolated and purified from the flower of Tussilago farfara
(1S,3aS,5R,7S,7aS)-1-[(1R)-1-Acetoxyethyl]-7-isopropyl-4-methylene-2-oxooctahydro-1H-inden-5-yl (2E)-3-methyl-2-pentenoate/Tussilagone//2-Pentenoic acid, 3-methyl-, (1S,3aS,5R,7S,7aS)-1-[(1R)-1-(acetyloxy)ethyl]octahydro-4-methylene-7-(1-methylethyl)-2-oxo-1H-inden-5-yl ester, (2E)-
471.3±35.0 °C at 760 mmHg
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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.
NF-κB; inflammation; macrophage; sepsis; tussilagone.
Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice
Yun Kyu Kim 1 , Myeong Gu Yeo 2 , Bo Kang Oh 3 , Ha Yeong Kim 4 , Hun Ji Yang 5 , Seung-Sik Cho 6 , Minchan Gil 7 , Kyung Jin Lee 8
2017 Dec 18
Inflammatory bowel disease (IBD) is a chronically relapsing inflammatory disorder of the gastrointestinal tract. Current IBD treatments are associated with poor tolerability and insufficient therapeutic efficacy, prompting the need for alternative therapeutic approaches. Recent advances suggest promising interventions based on a number of phytochemicals. Herein, we explored the beneficial effects of tussilagone, a major component of Tussilago farfara, in mice subjected to acute colitis induced by dextran sulfate sodium (DSS). Treatment with tussilagone resulted in a significant protective effect against DSS-induced acute colitis in mice via amelioration of weight loss, and attenuation of colonic inflammatory damage. Additionally, the expression of tumor necrosis factor-α and interleukin-6 and the activity of myeloperoxidase in colonic tissues were significantly reduced in tussilagone-treated mice. Furthermore, immunohistochemical analysis revealed that tussilagone treatment reduced the numbers of nuclear factor-kappa B (NF-κB) and increased the numbers of nuclear factor erythroid 2-related factor 2 (Nrf2) in nuclei of colonic tissues. Taken together, tussilagone treatment attenuated DSS-induced colitis in mice through inhibiting the activation of NF-κB and inducing Nrf2 pathways, indicating that tussilagone is a potent therapeutic candidate for treatment of intestinal inflammation.
Heme oxygenase-1; Inflammatory bowel disease; NF-κB; Nrf2; Tussilagone.
Tussilagone, a Major Active Component in Tussilago Farfara, Ameliorates Inflammatory Responses in Dextran Sulphate Sodium-Induced Murine Colitis
Hye Jin Cheon 1 , Sang-Hyeon Nam 1 , Jin-Kyung Kim 2
2018 Oct 1
In the present study, we investigated whether tussilagone, a natural product derived from Tussilago farfara, significantly affects the production and gene expression of airway MUC5AC mucin. Confluent NCI-H292 cells were pretreated with tussilagone for 30 min and then stimulated with EGF (epidermal growth factor) or PMA (phorbol 12-myristate 13-acetate) for 24 h or the indicated periods. The MUC5AC mucin gene expression was measured by RT-PCR. Production of MUC5AC mucin protein was measured by ELISA. To elucidate the action mechanism of tussilagone, effect of tussilagone on PMA-induced NF-κB signaling pathway was investigated by western blot analysis. Tussilagone significantly inhibited the production of MUC5AC mucin protein and down-regulated the expression of MUC5AC mucin gene, induced by EGF or PMA. Tussilagone inhibited PMA-induced activation (phosphorylation) of inhibitory kappa B kinase (IKK), and thus phosphorylation and degradation of inhibitory kappa Ba (IκBα). Tussilagone inhibited PMA-induced phosphorylation and nuclear translocation of nuclear factor kappa B (NF-κB) p65. This, in turn, led to the down-regulation of MUC5AC protein production in NCI-H292 cells. These results suggest that tussilagone can regulate the production and gene expression of mucin by acting on airway epithelial cells through regulation of NF-κB signaling pathway.
Airway; Epithelium; Gene expression; Mucin; Tussilagone.
Tussilagone Suppressed the Production and Gene Expression of MUC5AC Mucin via Regulating Nuclear Factor-Kappa B Signaling Pathway in Airway Epithelial Cells
Byung-Soo Choi 1 , Yu-Jin Kim 1 , Yong Pill Yoon 1 , Hyun Jae Lee 2 , Choong Jae Lee 1