Forsythin inhibits ß-hydroxybutyrate-induced oxidative stress in bovine macrophages by regulating p38/ERK, PI3K/Akt, and Nrf2/HO-1 signaling pathways.

Ketosis is a metabolic disease of dairy cows in the perinatal period, ß-hydroxybutyrate (ß-HB) is the main component of ketosis. High levels of ß-HB can trigger oxidative stress and inflammatory response in dairy cows, leading to decreased milk yield and multiple postpartum diseases. Forsythin (FOR), the major constituent of the herbal medicine Forsythia, has anti-inflammatory, anti-oxidant, and antiviral effects. FOR was demonstrated to have an antioxidant effect on PC12 cells. However, the effects of FOR on ß-HB-stimulated bovine macrophages (BMs) has not been reported. Thus, the aim of the present study was to investigate the effects of FOR on ß-HB-stimulated BMs. Firstly, the CCK8 test confirmed that FOR (50, 100, 200 µg/mL) has no effect on BMs activity, and we selected these concentrations for subsequent experiments. Secondly, through detecting the oxidation indexes ROS, MDA and antioxidant indexes CAT and SOD, we confirmed the antioxidant effect of FOR on BMs. Next, qRT-PCR confirmed that FOR dramatically reduced the mRNA levels of IL-1ß and IL-6. Furthermore, the western blotting confirmed that FOR observably down-regulated ß-HB-stimulated phosphorylation of p38, ERK and Akt and up-regulated expression of Nrf2, and HO-1. Above results suggested that FOR plays antioxidant effects on ß-HB-induced BMs through p38, ERK and PI3K/Akt, Nrf2 and HO-1 signaling pathways. Therefore, we speculated that FOR may be a potential medicine to alleviate ß-HB-induced inflammatory response and provide a preliminary reference for the research and development of FOR.

Selenium-Rich Yeast Mitigates Aluminum-Mediated Testicular Toxicity by Blocking Oxidative Stress, Inhibiting NO Production, and Disturbing Ionic Homeostasis.

Aluminum (Al) poisoning has been linked to the development of several reproductive system dysfunctions. Dietary supplementation with selenium-rich yeast (SeY) has been shown to prevent a variety of pathologic conditions. In the present study, the potential protect role of SeY on Al-induced testicular toxicity was evaluated, and the possible underlying mechanisms were discussed. Mice were treated with SeY (0.1 mg/kg) and/or Al (10 mg/kg) by oral gavage for 4 weeks. Histopathologic changes were observed in the testes of Al-treated mice. Oxidative stress, ionic disturbances, and the generation of NO systems are believed to have resulted in the observed pathology. Interestingly, SeY supplementation significantly inhibited the Al-induced histopathological and molecular changes and restored these indicators to levels observed in the control animals. These results suggest that SeY exerts a testis-protective effect against Al-induced toxicity through the reduction of oxidative stress, NO production, and the maintenance of ionic homeostasis.

Selenium-Rich Yeast Protects Against Aluminum-Induced Renal Inflammation and Ionic Disturbances.

The aim of this study was to evaluate the protective effects of SeY (selenium-rich yeast) against Al (aluminum)-induced inflammation and ionic imbalances. Male Kunming mice were treated with Al (10 mg/kg) and/or SeY (0.1 mg/kg) by oral gavage for 28 days. The degree of inflammation was assessed by mRNA expression of inflammatory biomarkers. Ionic disorders were assessed by determining the Na+, K+, and Ca2+ content, as well as the alteration in ATP-modifying enzymes (ATPases), including Na+K+-ATPase, Ca2+-ATPase, Mg2+-ATPase, Ca2+Mg2+-ATPase, and the mRNA levels of ATPase's subunits in kidney. It was observed here that SeY exhibited a significant protective effect on the kidney against the Al-induced upregulation of pro-inflammatory and downregulation of anti-inflammatory cytokines. Furthermore, a significant effect of Al on the Na+, K+, Ca2+, and Mg2+ levels in kidney was observed, and Al was observed to decrease the activities of Na+K+-ATPase, Mg2+-ATPase, and Ca2+Mg2+-ATPase. The mRNA expression of the Na+K+-ATPase subunits and Ca2+-ATPase subunits was regulated significantly by Al. Notably, SeY modulated the Al-induced alterations of ion concentrations, ATPase activity, and mRNA expression of their subunits. These results suggest that SeY prevents renal toxicity caused by Al via regulation of inflammatory responses, ATPase activities, and transcription of their subunits.