Monascus-fermented metabolites repressed amyloid β-peptide-induced neurotoxicity and inflammatory response in in vitro and in vivo studies

Monascus purpureus-produced monascin (MS) and ankaflavin (AK) have the potential to improve memory deficiency in Alzheimer's disease rat models; however, the mechanisms are still unclear. We aimed to investigate the effects and mechanisms of MS and AK on preventing Aβ40-induced oxidative stress...

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Main Authors: Che-Wei Lin, Pei-Ying Lin, Ya-Wen Hsu, Tzu-Ming Pan, Chun-Lin Lee
Format: Article
Language:English
Published: Elsevier 2023-05-01
Series:Journal of Functional Foods
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S1756464623001093
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author Che-Wei Lin
Pei-Ying Lin
Ya-Wen Hsu
Tzu-Ming Pan
Chun-Lin Lee
author_facet Che-Wei Lin
Pei-Ying Lin
Ya-Wen Hsu
Tzu-Ming Pan
Chun-Lin Lee
author_sort Che-Wei Lin
collection DOAJ
description Monascus purpureus-produced monascin (MS) and ankaflavin (AK) have the potential to improve memory deficiency in Alzheimer's disease rat models; however, the mechanisms are still unclear. We aimed to investigate the effects and mechanisms of MS and AK on preventing Aβ40-induced oxidative stress and inflammatory response through in vitro and in vivo studies. Aβ40-treated PC-12 cells and intracerebroventricularly Aβ40-infused rats were used as the in vitro and in vivo models, respectively. MS and AK enhanced cell viability in Aβ40-treated PC-12 cells. Furthermore, the expression levels of oxidative and inflammatory factors, including COX-2, IL-1β, IL-6, iNOS, NF-κB, and TNF-α, were repressed by MS and AK treatment in the in vitro and in vivo models. The anti-oxidative and anti-inflammatory effects were the probable reasons for repressing Aβ40-induced p-tau protein expression, Aβ fibrils formation, neurotoxicity, and memory deficiency.
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spelling doaj.art-b9a8f518ad024e1eb2dfca22e02a4b7a2023-04-29T14:48:21ZengElsevierJournal of Functional Foods1756-46462023-05-01104105509Monascus-fermented metabolites repressed amyloid β-peptide-induced neurotoxicity and inflammatory response in in vitro and in vivo studiesChe-Wei Lin0Pei-Ying Lin1Ya-Wen Hsu2Tzu-Ming Pan3Chun-Lin Lee4SunWay Biotech Co., Taipei, Taiwan, ROCSunWay Biotech Co., Taipei, Taiwan, ROC; Department of Life Science, National Taitung University, 369, Sec. 2, University Rd., Taitung 95092, Taiwan, ROCSunWay Biotech Co., Taipei, Taiwan, ROCSunWay Biotech Co., Taipei, Taiwan, ROC; Department of Biochemical Science and Technology, National Taiwan University, Taiwan, ROC; Corresponding authors at: Department of Life Science, National Taitung University, 369, Sec. 2, University Rd., Taitung 95092, Taiwan, ROC (C.-L. Lee). Department of Biochemical Science & Technology, National Taiwan University, Taiwan, ROC (T.-M. Pan).Department of Life Science, National Taitung University, 369, Sec. 2, University Rd., Taitung 95092, Taiwan, ROC; Corresponding authors at: Department of Life Science, National Taitung University, 369, Sec. 2, University Rd., Taitung 95092, Taiwan, ROC (C.-L. Lee). Department of Biochemical Science & Technology, National Taiwan University, Taiwan, ROC (T.-M. Pan).Monascus purpureus-produced monascin (MS) and ankaflavin (AK) have the potential to improve memory deficiency in Alzheimer's disease rat models; however, the mechanisms are still unclear. We aimed to investigate the effects and mechanisms of MS and AK on preventing Aβ40-induced oxidative stress and inflammatory response through in vitro and in vivo studies. Aβ40-treated PC-12 cells and intracerebroventricularly Aβ40-infused rats were used as the in vitro and in vivo models, respectively. MS and AK enhanced cell viability in Aβ40-treated PC-12 cells. Furthermore, the expression levels of oxidative and inflammatory factors, including COX-2, IL-1β, IL-6, iNOS, NF-κB, and TNF-α, were repressed by MS and AK treatment in the in vitro and in vivo models. The anti-oxidative and anti-inflammatory effects were the probable reasons for repressing Aβ40-induced p-tau protein expression, Aβ fibrils formation, neurotoxicity, and memory deficiency.http://www.sciencedirect.com/science/article/pii/S1756464623001093MonascinAnkaflavinAlzheimer's diseaseAmyloid β-peptideMonascusInflammatory
spellingShingle Che-Wei Lin
Pei-Ying Lin
Ya-Wen Hsu
Tzu-Ming Pan
Chun-Lin Lee
Monascus-fermented metabolites repressed amyloid β-peptide-induced neurotoxicity and inflammatory response in in vitro and in vivo studies
Journal of Functional Foods
Monascin
Ankaflavin
Alzheimer's disease
Amyloid β-peptide
Monascus
Inflammatory
title Monascus-fermented metabolites repressed amyloid β-peptide-induced neurotoxicity and inflammatory response in in vitro and in vivo studies
title_full Monascus-fermented metabolites repressed amyloid β-peptide-induced neurotoxicity and inflammatory response in in vitro and in vivo studies
title_fullStr Monascus-fermented metabolites repressed amyloid β-peptide-induced neurotoxicity and inflammatory response in in vitro and in vivo studies
title_full_unstemmed Monascus-fermented metabolites repressed amyloid β-peptide-induced neurotoxicity and inflammatory response in in vitro and in vivo studies
title_short Monascus-fermented metabolites repressed amyloid β-peptide-induced neurotoxicity and inflammatory response in in vitro and in vivo studies
title_sort monascus fermented metabolites repressed amyloid β peptide induced neurotoxicity and inflammatory response in in vitro and in vivo studies
topic Monascin
Ankaflavin
Alzheimer's disease
Amyloid β-peptide
Monascus
Inflammatory
url http://www.sciencedirect.com/science/article/pii/S1756464623001093
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