ABSTRACT
BACKGROUND: Glycerophospholipids were the main components of cerebral cortex lipids, and there was a close association between lipid homeostasis and human health. It has been reported that dietary DHA-enriched phosphatidylcholine (DHA-PC) and phosphatidylserine (DHA-PS) could improve brain function. However, it was unclear that whether supplementation of DHA-PC and DHA-PS could change lipid profiles in the brain of dementia animals. METHODS: SAMP8 mice was fed with different diet patterns for 2 months, including high-fat diet and low-fat diet. After intervention with DHA-PC and DHA-PS for another 2 months, the lipid profile in cerebral cortex was determined by lipidomics in dementia mice. RESULTS: High-fat diet could significantly decrease the levels of DHA-containing PS/pPE, DPA-containing PS, and AA-containing PE, which might exhibit the potential of lipid biomarkers for the prevention and diagnosis of AD. Notably, DHA-PC and DHA-PS remarkably recovered the lipid homeostasis in dementia mice. These might provide a potential novel therapy strategy and direction of dietary intervention for patients with cognitive decline. CONCLUSIONS: DHA-PC and DHA-PS could recover the content of brain DHA-containing PS and pPE in SAMP8 mice fed with high-fat diet.
Subject(s)
Cerebral Cortex/chemistry , Diet, High-Fat , Docosahexaenoic Acids/analysis , Phosphatidylcholines/chemistry , Phosphatidylserines/analysis , Plasmalogens/analysis , Alzheimer Disease , Animals , Cerebral Cortex/drug effects , Disease Models, Animal , Lipidomics , Male , Mice , Phosphatidylcholines/pharmacology , Phosphatidylserines/chemistry , Phosphatidylserines/metabolism , Phosphatidylserines/pharmacology , Plasmalogens/chemistry , Plasmalogens/metabolismABSTRACT
OBJECTIVES: Astragaloside IV, purified from the Chinese medical herb Astragalus membranaceus (Fisch) Bge and Astragalus caspicus Bieb, is an important natural product with multiple pharmacological actions. This study investigated the anti-ADVs effect of astragaloside IV on HAdV-3 (human adenovirus type 3) in A549 cell. METHODS: CPE, MTT, quantitative real-time PCR (qPCR), flow cytometry (FCM) and Western blot were apply to detect the cytotoxicity, the inhibition and the mechanisms of astragaloside IV on HAdV-3. KEY FINDINGS: TC(0 ) of astragaloside IV was 116.8 µm, the virus inhibition rate from 15.98% to 65.68% positively was correlated with the concentration of astragaloside IV from 1.25 µm to 80 µm, IC50 (the medium inhibitory concentration) was 23.85 µm, LC50 (lethal dose 50% concentration) was 865.26 µm and the TI (therapeutic index) was 36.28. qPCR result showed astragaloside IV inhibited the replication of HAdV-3. Flow FCM analysis demonstrated that the anti-HAdV-3 effect was associated with apoptosis. Astragaloside IV was further detected to reduce the protein expressions of Bax and Caspase-3 and increasing the protein expressions of Bcl-2 using western blotting, which improved the anti-apoptosis mechanism of astragaloside IV on HAdV-3. CONCLUSIONS: Our findings suggested that astragaloside IV possessed anti-HAdV-3 capabilities and the underlying mechanisms might involve inhibiting HAdV-3 replication and HAdV-3-induced apoptosis.