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Two new lanostane triterpenoid acids, 12β, 15α-dihydroxy-24-methyl-3,23-dioxo-lanosta-7,9(11)-dien-26-oic acid (1), and 3α, 12β-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.

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.

Zearalenone (ZEN) exerts a major effect on human and animal health and has led to serious worldwide economic problems. In this study, we investigated whether proanthocyanidin (PC) can prevent ZEN-induced testicular oxidative damage in male mice and explored the underlying mechanism. Kunming mice were injected with ZEN (40 mg kg-1) on the 11th day after intragastric administration of PC (75 or 150 mg/kg) for 10 days; the sperm quality of mice was then analysed statistically. Additionally, testicular morphology parameters related to oxidative damage, apoptosis and the expression of endoplasmic reticulum (ER) stress-related genes (GRP78, CHOP and XBP-1) were all measured. Results showed that ZEN exposure significantly reduced the sperm density, improved the sperm aberration rate, increased the MDA level and reduced SOD and GSH-Px activities. Meanwhile, ZEN was attributed to the downregulation of the expressions of the gene and protein of Bcl-2 and upregulation of the expressions of the gene and protein of Bax and caspase-3. ZEN exposure also upregulated the mRNA expression of GRP78, CHOP and XBP-1; however, PC pre-treatment reduced ZEN-induced oxidative damage and tended to maintain normal testicular morphology. Furthermore, PC pre-treatment substantially downregulated the expressions of the GRP78, CHOP and XBP-1 and upregulated the expression of the Bcl-2 gene. In conclusion, PC, due to its anti-oxidative ability, could ameliorate ZEN-induced testicular reproductive toxicity in male mice by decreasing ER stress and testicular cell apoptosis.