eclalbasaponin-i has been researched along with echinocystic-acid* in 2 studies
2 other study(ies) available for eclalbasaponin-i and echinocystic-acid
| Article | Year |
|---|---|
Eclalbasaponin II induces autophagic and apoptotic cell death in human ovarian cancer cells.
Triterpenoids echinocystic acid and its glycosides, isolated from several Eclipta prostrata, have been reported to possess various biological activities such as anti-inflammatory, anti-bacterial, and anti-diabetic activity. However, the cytotoxicity of the triterpenoids in human cancer cells and their molecular mechanism of action are poorly understood. In the present study, we found that eclalbasaponin II with one glucose moiety has potent cytotoxicity in three ovarian cancer cells and two endometrial cancer cells compared to an aglycone echinocystic acid and eclalbasaponin I with two glucose moiety. Eclalbasaponin II treatment dose-dependently increased sub G Topics: Antineoplastic Agents; Apoptosis; Autophagy; Cell Line, Tumor; Female; Humans; JNK Mitogen-Activated Protein Kinases; Oleanolic Acid; Ovarian Neoplasms; p38 Mitogen-Activated Protein Kinases; Saponins; TOR Serine-Threonine Kinases | 2016 |
Echinocystic acid isolated from Eclipta prostrata suppresses lipopolysaccharide-induced iNOS, TNF-α, and IL-6 expressions via NF-κB inactivation in RAW 264.7 macrophages.
In this study, we aimed to identify the compounds in Eclipta prostrata responsible for its anti-inflammatory effects using an in vitro bioassay. Three triterpenoids, eclalbasaponin I, eclalbasaponin II, and echinocystic acid, were isolated from an EtOAc fraction of the 70 % EtOH extract of E. prostrata by activity-guided fractionation based on the inhibition of nitric oxide release from lipopolysaccharide-induced RAW 264.7 macrophages. Of these three triterpenoids, echinocystic acid inhibited lipopolysaccharide-induced production of nitric oxide and cytokines such as tumor necrosis factor-α and interleukin-6. Consistent with these observations, echinocystic acid concentration-dependently inhibited lipopolysaccharide-induced inducible nitric oxide synthase expression at the protein level and inducible nitric oxide synthase, tumor necrosis factor-α, and interleukin-6 expression at the mRNA level, and inhibited lipopolysaccharide-induced iNOS promoter binding activity. In addition, echinocystic acid suppressed the lipopolysaccharide-induced transcriptional activity of nuclear factor-κB by blocking the nuclear translocation of p65. Topics: Animals; Anti-Inflammatory Agents; Cell Line; Down-Regulation; Eclipta; Gene Expression Regulation; Interleukin-6; Lipopolysaccharides; Macrophages; Mice; NF-kappa B; Nitric Oxide Synthase Type II; Oleanolic Acid; Plants, Medicinal; Saponins; Triterpenes; Tumor Necrosis Factor-alpha | 2013 |