[Chemical constituents from traditional Uighur herbal medicine Elaeagnus angustifolia flowers].

Seven aromatic glycosides (1-7), including four phenylethanol glycosides, one phenylmethanol glycoside, one phenylpropane glycoside and one benzoside, were isolated from the methanolic extract of Uighur Medicine Elaeagnus angustifolia flowers. Their structures were elucidated based on the analysis of spectroscopic data (1D, 2D NMR and HR-MS). Compound 1 is a new compound, named as angustifol A. Six known compounds were identified as 2-phenylethyl-O-ß-D-glucopyranoside(2), salidroside (3), vanillic acid 4-O-ß-D-glucopyranoside(4), vanilloloside (5), (Z)-isoconiferin (6), 2-phenylethyl-6-O-α-L-arabinofuranosyl-ß-D-glucopyranoside (7). Compounds 2-7 were isolated from the genus Elaeagnus for the first time. In vitro anti-inflammatory assays revealed that none of these compounds showed good COX inhibitory activities.

[Two new triterpenoid acids from Uighur medicine Fomes officinalis].

Two new lanostane triterpenoid acids, 12ß, 15α-dihydroxy-24-methyl-3,23-dioxo-lanosta-7,9(11)-dien-26-oic acid (1), and 3α, 12ß-dihydroxy-24-methyl-7,23-dioxo-lanosta-8-en-26-oic acid (2), were isolated from the methanolic extract of Uighur medicine Fomes officinalis. Their structures were elucidated based on the analysis of spectroscopic data (1D, 2D NMR and HR-MS). Anti-inflammatory and cytotoxicity assays revealed that both compound 1 and 2 show no inhibitory effects on nitric oxide production in lipopolysaccharide-induced RAW264.7 cells, and no cytotoxicity activities against HepG2 cells.

The Protective Effect of Grape-Seed Proanthocyanidin Extract on Oxidative Damage Induced by Zearalenone in Kunming Mice Liver.

Although grape-seed proanthocyanidin extract (GSPE) demonstrates strong anti-oxidant activity, little research has been done to clearly reveal the protective effects on the hepatotoxicity caused by zearalenone (ZEN). This study is to explore the protective effect of GSPE on ZEN-induced oxidative damage of liver in Kunming mice and the possible protective molecular mechanism of GSPE. The results indicated that GSPE could greatly reduce the ZEN-induced increase of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities. GSPE also significantly decreased the content of MDA but enhanced the activities of antioxidant enzymes SOD and GSH-Px. The analysis indicated that ZEN decreased both mRNA expression levels and protein expression levels of nuclear erythroid2-related factor2 (Nrf2). Nrf2 is considered to be an essential antioxidative transcription factor, as downstream GSH-Px, γ-glutamyl cysteine synthetase (γ-GCS), hemeoxygenase-1 (HO-1), and quinone oxidoreductase 1 (NQO1) decreased simultaneously, whereas the pre-administration of GSPE groups was shown to elevate these expressions. The results indicated that GSPE exerted a protective effect on ZEN-induced hepatic injury and the mechanism might be related to the activation of the Nrf2/ARE signaling pathway.

Intervention of Grape Seed Proanthocyanidin Extract on the Subchronic Immune Injury in Mice Induced by Aflatoxin B1.

The aim was to investigate the prevention of grape seed proanthocyanidin extract (GSPE) on the subchronic immune injury induced by aflatoxin B1 (AFB1) and the possible ameliorating effect of GSPE in mice. The subchronic AFB1-induced immune injury mice model was set up with the continuous administration of 100 µg/kg body weight (BW) AFB1 for six weeks by intragastric administration. Then, intervention with different doses (50 and 100 mg/kg BW) of GSPE was conducted on mice to analyze the changes of body weight, immune organ index, antioxidant capability of spleen, serum immunoglobulin content, and the expression levels of inflammatory cytokines. The prevention of GSPE on the immune injury induced by AFB1 was studied. The GSPE could relieve the AFB1-induced reduction of body weight gain and the atrophy of the immune organ. The malondialdehyde (MDA) level of the spleen in the AFB1 model group significantly increased, but levels of catalase (CAT), glutathione (GSH), glutathione peroxidase (GSH-P(X)), and superoxide dismutase (SOD) significantly decreased. The GSPE could significantly inhibit the oxidative stress injury of the spleen induced by AFB1. AFB1 exposure could not significantly change the contents of IgA, IgG, or IgM. AFB1 significantly improved the expression of interleukin 1ß (IL-1ß), IL-6, tumor necrosis factor α (TNF-α), and interferon γ (IFN-γ). Additionally, GSPE could decrease the expression of these four proinflammatory factors to different degrees and inhibit the inflammatory reaction of mice. The results suggest that GSPE alleviates AFB1-induced oxidative stress and significantly improves the immune injury of mice induced by AFB1.