Fermented black radish (Raphanus sativus L. var. niger) attenuates methionine and choline deficient diet-induced nonalcoholic fatty liver disease in mice.

As one of the wide-ranging form of chronic liver disease, there are only limited therapeutic options for nonalcoholic fatty liver disease (NAFLD). We evaluated whether fermented black radish (Raphanus sativus L. var. niger; FBR) ameliorates lipid accumulation, inflammation, and hepatic fibrosis, which are characteristics of the pathogenesis of NAFLD. Fermented black radish treatment reduced lipid accumulation in 3T3-L1 adipocytes, which appeared to be associated with the downregulation of adipogenic transcription factors, including sterol regulatory element-binding protein 1c, CCAAT/enhancer-binding protein α, peroxisome proliferator-activated receptor γ, and lipid accumulation-related genes including adipocyte protein-2 and fatty acid synthase. Administration of FBR to C57BL/6J mice challenged with methionine and choline deficient (MCD) diet significantly attenuated the increased serum levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and triglyceride. In addition, treatment with FBR interestingly repressed the hepatic inflammation induced with MCD diet, by lowering the expression of inducible nitric oxide synthase and suppressing the inactivation of macrophages and Kupffer cells in the liver. Fermented black radish was also shown to mitigate liver fibrosis through the inhibition of alpha-smooth muscle actin, transforming growth factor beta-1, and collagen type I alpha 1 chain. Our results indicate that FBR ameliorates NAFLD and its related metabolic disease by regulating multiple pathways, suggesting that FBR may be an effective dietary supplement for ameliorating NAFLD.

Zeatin prevents amyloid beta-induced neurotoxicity and scopolamine-induced cognitive deficits.

The antioxidative and protective effects of zeatin against amyloid beta-protein (Abeta)-induced neurotoxicity were investigated using PC12 cells. Zeatin showed antioxidative and cell protective effects against Abeta-induced neurotoxicity. In this study, we also evaluated the effect of zeatin on learning and memory capacity in vivo using ICR mice with amnesia induced by scopolamine (1 mg/kg of body weight). Zeatin, when administered to mice at 4.5 mg/kg of body weight, significantly ameliorated scopolamine-induced amnesia as measured in both the passive avoidance test and Y-maze test. Injecting mice with scopolamine impaired performance on the passive avoidance test (48 +/- 4.5% decrease) and on the Y-maze test (12 +/- 1.3% decrease). In contrast, mice treated with zeatin before scopolamine injections were protected from these changes (5-34% decrease in step-through latency; 1-4% decrease in alternation behavior). The present results suggest a possible chemopreventive role of zeatin in Alzheimer's disease.