| Biochem Biophys Res Commun. 2014 Jan 3;443(1):132-7. |
| Tussilagone suppresses colon cancer cell proliferation by promoting the degradation of β-catenin.[Pubmed: 24269588] |
Abnormal activation of the Wnt/β-catenin signaling pathway frequently induces colon cancer progression.
METHODS AND RESULTS:
In the present study, we identified tussilagone (TSL), a compound isolated from the flower buds of Tussilago farfara, as an inhibitor on β-catenin dependent Wnt pathway. TSL suppressed β-catenin/T-cell factor transcriptional activity and down-regulated β-catenin level both in cytoplasm and nuclei of HEK293 reporter cells when they were stimulated by Wnt3a or activated by an inhibitor of glycogen synthase kinase-3β. Since the mRNA level was not changed by TSL, proteasomal degradation might be responsible for the decreased level of β-catenin. In SW480 and HCT116 colon cancer cell lines, TSL suppressed the β-catenin activity and also decreased the expression of cyclin D1 and c-myc, representative target genes of the Wnt/β-catenin signaling pathway, and consequently inhibited the proliferation of colon cancer cells.
CONCLUSIONS:
Taken together, TSL might be a potential chemotherapeutic agent for the prevention and treatment of human colon cancer. |
| Arch Pharm Res. 2008 May;31(5):645-52. |
| Suppression of inducible nitric oxide synthase and cyclooxygenase-2 expression by tussilagone from Farfarae flos in BV-2 microglial cells.[Pubmed: 18481023] |
Activated microglia produce diverse neurotoxic factors such as nitric oxide (NO) and prostaglandin E(2) (PGE(2)) that may cause neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease.
METHODS AND RESULTS:
From the EtOAc soluble fraction of Farfarae flos (Tussilago farfara), we purified tussilagone as a bioactive compound by monitoring the inhibitory potential of NO production in activated microglia through the purification procedures. Tussilagone showed dose-dependent inhibition of NO and PGE(2) production in LPS-activated microglia with IC(50) values of 8.67 microM and 14.1 microM, respectively. It suppressed the expression of protein and mRNA of inducible nitric oxide synthase and cyclooxygenase-2 through the inhibition of 1-kappaBalpha degradation and nuclear translocation of p65 subunit of NF-kappaB.
CONCLUSIONS:
Therefore tussilagone from Farfarae flos may have therapeutic potential in the treatment of neuro-inflammatory diseases through the inhibition of overproduction of NO and PGE(2). |
| Chem Biol Interact . 2018 Oct 1;294:74-80. |
| Tussilagone, a major active component in Tussilago farfara, ameliorates inflammatory responses in dextran sulphate sodium-induced murine colitis[Pubmed: 30142311] |
| Abstract
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. |
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