Acetyl oleanolic acid aldehyde

The antioxidative compounds were extracted by ultrasonic treatment of bran extracts of seven pigmented (completely) and non pigmented (sparsely) colored rice cultivars followed by assessment of their in vitro antioxidative capacity by LC-MS and oxidation/reduction assay based methods. A total of 40-compounds, 7-phenolic, 9-flavonoids, 9-hydroxycinammic acid derivatives, 3-hydroxybenzoic acid derivatives and other glucosides specifically, pro-anthocyanidin trimer and procyanidin-B1 (dimer) were indentified in completely colored rice cultivars. Higher DPPH radical scavenging activity of pigmented cultivars was due to higher percentage of phenolics like thymol, quinicquinic-caffeicacid ester and polar dicaffeoylquinic acid; whereas higher lipid peroxidation inhibition was attributed to the presence of polar substances such as p-hydroxybenzoicacid, procyanidin B1 and quercetin-3-O-rutinoside. The phosphomolybdenum reduction capacity was attributed to luteolin-7-O-glucoside, apigenin-7-O-glucoside, caffeicacid, myrecitin and phloreticacid. Whereas, grater reducing power of pigmented bran was attributed to presence of multiple-OH groups containing phenols, flavonoid and hydracinammicacid depicting potential health and nutritional effects of these rice cultivars.

The aim of the present work is to isolate a series of triterpene derivatives with rhamnosyl linking acetyl groups from Glechoma longituba according to the structural characteristics of previously described triterpene saponins. The extract ion chromatography spectrum of the crude extract of G. longituba was detected and analyzed by HPLC-HR-ESI-MS to determine possible components, and these metabolites were traced and separated by combining high-resolution mass spectrometry and predicted liquid chromatography retention time. Three 11α, 12α-epoxypentacyclic oleanolic acid triterpene saponins (glechomanosides H-J) and one ursane triterpene aldehyde saponin with a C-28 aldehyde group were isolated from G. longituba. The structure of these compounds was confirmed by NMR and compared with those of previously characterized compounds. The strategy described in this report enables a rapid, reliable, and complete analysis of glycoside compounds containing different numbers of acetyl groups at different positions on the sugar.

We and others have recently shown that soyasaponins abundant in soybeans can decrease inflammation by suppressing the nuclear factor kappa B (NF-kB)-mediated inflammation. However, the exact molecular mechanisms by which soyasaponins inhibit the NF-kB pathway have not been established. In this study in macrophages, soyasaponins (A1, A2 and I) inhibited the lipopolysaccharide (LPS)-induced release of inflammatory marker prostaglandin E2 (PGE2) to a similar extent as the NF-kB inhibitor (BAY117082). Soyasaponins (A1, A2 and I) also suppressed the LPS-induced expression of cyclooxygenase 2 (COX-2), another inflammatory marker, in a dose-dependent manner by inhibiting NF-kB activation. In defining the associated mechanisms, we found that soyasaponins (A1, A2 and I) blunted the LPS-induced IKKα/β phosphorylation, IkB phosphorylation and degradation, and NF-kB p65 phosphorylation and nuclear translocation. In studying the upstream targets of soyasaponins on the NF-kB pathway, we found that soyasaponins (A1, A2 and I) suppressed the LPS-induced activation of PI3K/Akt similarly as the PI3K inhibitor LY294002, which alone blocked the LPS-induced activation of NF-kB. Additionally, soyasaponins (A1, A2 and I) reduced the LPS-induced production of reactive oxygen species (ROS) to the same extent as the anti-oxidant N-acetyl-L-cysteine, which alone inhibited the LPS-induced phosphorylation of Akt, IKKα/β, IkBα, and p65, transactivity of NF-kB, PGE2 production, and malondialdehyde production. Finally, our results show that soyasaponins (A1, A2 and I) elevated SOD activity and the GSH/GSSG ratio. Together, these results show that soyasaponins (A1, A2 and I) can blunt inflammation by inhibiting the ROS-mediated activation of the PI3K/Akt/NF-kB pathway.