Red mold rice extract represses amyloid β peptide-induced neurotoxicity via potent synergism of anti-inflammatory and antioxidative effect

Amyloid β-peptide (Aβ), a risk of Alzheimer's disease (AD), causes cell death by inflammation and oxidative stress. Red mold rice (RMR) fermented by Monascus species is regarded as cholesterol-lowering functional food in virtue of the metabolite monacolin K identified as lovastatin. In addition, RMR is also demonstrated to express antioxidation because of multiple antioxidants.Therefore, this study focuses on the synergism of RMR against Aβ neurotoxicity and compares the effect between lovastatin and RMR including monacolin K andother functional metabolites. In this study, RE 568, an ethanol extract of RMR produced by strain Monascus purpureus NTU 568, is used to protect PC12 cell against Aβ40 neurotoxicity. All tests contain the treatments with lovastatin or RE 568 including equal monacolin K levels inorder to compare the effect and investigate whether other metabolites of RE 568 provide potent assistance against Aβ40 neurotoxicity. In the results, monacolin K represses Aβ40 neurotoxicity via repressing small G-protein-mediated inflammation, and other metabolites of RE 568 also exhibit potent antioxidative ability against Aβ-induced oxidative stress. Importantly, stronger effects on repressing the Aβ40-induced cell death, inflammation, and oxidative stress are performed by RE 568 than that by the equal levels of lovastatin, which results from a potent synergism made up of monacolin K, antioxidants, and anti-inflammatory agents. The present study is the first report to demonstrate the potent synergistic protection of RMR against Aβ40 neurotoxicity, which would cause RMR to be developed as potential and novel functional food for the prophylaxis of AD pathogenesis.