Alzheimer＇s disease （AD） is one of the most common cognitive disorders of the elderly. Fucoxanthin is a carotenoid that is found in common edible seaweed, and it is considered as a major active compound of marine algae with cancer-preventing, antioxidant and anti-inflammatory properties. In this study, we investigated the ability of fucoxanthin to protect against the β-amyloid protein （Aβ）-induced neurotoxicity in primary cortical cultured neurons and PC12 cells. Neuroprotective effects of fucoxanthin were determined by measuring cell viability and nuclei double-staining with Hoechst 33342 and propidium iodide following Aβ treatment with or without fucoxanthin. Moreover, we also evaluated its potential mechanism on antioxidation by detecting the total antioxidant capacity （T-AOC）, level of lipid peroxidation malondialdehyde （MDA） and activity of superoxide dismutase （SOD）. We found that exposure of cortical cultured neurons or PC12 cells to Aβ resulted in neuronal cell death, whereas pre-treatment with fucoxanthin reduced Aβ-induced cell death. The data on the T-AOC, MDA level and SOD activity showed that Aβ treatment resulted in decreases in T-AOC and SOD activity and an increase in MDA level. After fucoxanthin administration, the results of T-AOC, MDA level and SOD activity showed an opposite trend, indicating that T-AOC was increased and MDA level was reduced. These results suggested that fucoxanthin prevented Aβ-induced neurotoxicity through attenuating oxidative stress induced by Aβ. Therefore, fucoxanthin might be useful as a potential preventive or theraoeutic agent for AD.
Salvia miltiorrhiza （Sm） is a traditional herbal medicine with multiple effects on various diseases. Its water-soluble parts have been used to produce injectional powder. In this study, liver fibrosis rats were induced by intraperitoneal injection of dimethylnitrosarnine for 3 consecutive days per week for 4 weeks. After 2 weeks, rats in the positive drug group were subcutaneously injected with 8×10^5 IU/kg IFNα2b, while the Sm treatment groups were intraperitoneally injected with 50, 100 and 200 mg/kg solution of Sm injectional powder, respectively, for 6 days per week for 4 weeks. The results showed that either IFNα2b or the Sm injectional powder significantly increased the body weight and liver to spleen ratio, and three doses of the powder brought down the spleen index. Serum analysis showed that both IFNα2b and the Sm powder reduced levels of alanine transaminase and total bilirubin, while only 100 and 200 mg/kg of the Sm powder ameliorated aspartate transaminase and albumin levels. In the collagen examination, reduced hyaluronic acid and procollagen type III levels, less fibrous hyperplasia and collagen deposits, and improved hepatocyte states were clearly observed in rats treated with either IFNα2b or Sm injectional powder. In addition, the mechanism of action of the Sm powder was also studied. Immunohistochemical staining showed that IFNα2b and Sm injectional powder significantly down-regulated the expression of transforming growth factor-β1 （TGF-β1） and platelet derived growth factor （PDGF）. In conclusion, Sm injectional powder has protective effects on dimethylnitrosamine-initiated liver fibrosis in rats, and the mechanism may include the down-regulation of TGF-β1 and PDGF.
