Natural Products from Ligularia fischeri

Isolation, Structure Elucidition, and Immunosuppressive Activity of Diterpenoids from Ligularia fischeri.[Pubmed: 28783337]

None

4,5-Di-O-Caffeoylquinic Acid from Ligularia fischeri Suppresses Inflammatory Responses Through TRPV1 Activation.[Pubmed: 28782267]

None

Chemical Lineages of Ligularia fischeri.[Pubmed: 27032186]

Six Ligularia fischeri samples, two from Sichuan (samples 1 and 2) and four from Chongqing (samples 3-6), were examined for root chemicals and the DNA sequence of the internal transcribed spacers of the ribosomal RNA gene. Samples 2 and 3 contained benzofurans. The isolation of benzofurans shows that the chemical diversity in L. fischeri is higher than previously reported. Samples 1, 4, 5, and 6 contained eremophilanes. However, the compounds were different between sample 1 and samples 4-6, indicating variation within eremophilane producers. DNA data indicated that introgression could be a mechanism of benzofuran production in sample 2 and that sample 1 and samples 4-6 were genetically separate.

5-Caffeoylquinic acid inhibits invasion of non-small cell lung cancer cells through the inactivation of p70S6K and Akt activity: Involvement of p53 in differential regulation of signaling pathways.[Pubmed: 26984670]

In the present study, we investigated the effects and molecular mechanism of 5-caffeoylquinic acid (5-CQA), a natural phenolic compound isolated from Ligularia fischeri, on cell invasion, proliferation and adhesion in p53 wild-type A549 and p53-deficient H1299 non-small cell lung cancer (NSCLC) cells. 5-CQA abrogated mitogen-stimulated invasion, but not proliferation, in both A549 and H1299 cells. In addition, 5-CQA inhibited mitogen-stimulated adhesion in A549 cells only. Anti-invasive activity of 5-CQA in A549 cells was mediated by the inactivation of p70(S6K)-dependent signaling pathway. In contrast, in H1299 cells the inactivation of Akt was found to be involved in 5-CQA-mediated inhibition of cell invasion. Collectively, these findings demonstrate the pharmacological roles and molecular targets of 5-CQA in regulating NSCLC cell fate, and suggest further evaluation and development of 5-CQA as a potential therapeutic agent for the treatment and prevention of lung cancer.

Ligularia fischeri extract attenuates liver damage induced by chronic alcohol intake.[Pubmed: 26799831]

Context Ligularia fischeri (Ledebour) Turcz. (Compositae) has been used as a leafy vegetable and in traditional medicine to treat hepatic disorder in East Asia. Objective The present study explores the antioxidant activity of LF aqueous extract on EtOH-induced oxidative stress accompanied by hepatotoxicity both in vitro and in vivo. Materials and methods In vitro study using the mouse liver NCTC-1469 cell line was conducted to estimate the cytotoxicity as well as the inhibitory effect of LF extract against alcohol-treated cell damage. In vivo study used an alcohol-fed Wister rat model orally administered EtOH (3.95 g/kg of body weight/d) with or without LF extract (100 or 200 mg/kg body weight) for 6 weeks. Serum and liver tissue were collected to evaluate hepatic injury and antioxidant-related enzyme activity. Results The EC50 value for the DPPH radical scavenging capacity of LF extract was 451.5 μg/mL, whereas the IC50 value of LF extract in terms of EtOH-induced reactive oxygen species (ROS) generation was 98.3 μg/mL without cell cytotoxicity. LF extract (200 mg/kg body weight) significantly reduced the triglyceride content of serum (33%) as well as hepatic lipid peroxidation (36%), whereas SOD activity was elevated three-fold. LF extract suppressed expression of CYP2E1 and TNF-α, and attenuated alcohol-induced abnormal morphological changes. Discussion and conclusion LF extract attenuated liver damage induced by alcoholic oxidative stress through inhibition of ROS generation, down-regulation of CYP2E1, and activation of hepatic antioxidative enzymes. Homeostasis of the antioxidative defence system in the liver by LF extract mitigated hepatic disorder following chronic alcohol intake.