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

Amyloid beta-peptide (A beta), 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 A beta neurotoxicity and compares the effect between lovastatin and RMR including monacolin K and other 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 A beta 40 neurotoxicity. All tests contain the treatments with lovastatin or RE 568 including equal monacolin K levels in order to compare the effect and investigate whether other metabolites of RE 568 provide potent assistance against A beta 40 neurotoxicity. In the results, monacolin K represses A beta 40 neurotoxicity via repressing small G-protein-mediated inflammation, and other metabolites of RE 568 also exhibit potent antioxidative ability against A beta-induced oxidative stress. Importantly, stronger effects on repressing the A beta 40-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 A beta 40 neurotoxicity, which would cause RMR to be developed as potential and novel functional food for the prophylaxis of AD pathogenesis.