Department of Neuro-health Innovation, Institute for Biomedical Sciences, Interdisciplinary Cluster for Cutting Edge Research, Shinshu University, Matsumoto, Japan; Department of Pathology, the Xiehe Hospital of Tangshan, Tangshan, China
Ying Li
Aging Biology, Department of Biomedical Engineering, Graduate School of Medicine, Science and Technology Shinshu University, Matsumoto, Japan
Fuyuki Kametani
Department of Dementia and Higher Brain Function, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan
Xiaoran Cui
Department of Aging Biology, Institute of Pathogenesis and Disease Prevention, Shinshu University Graduate School of Medicine, Matsumoto, Japan
Yuichi Igarashi
Department of Aging Biology, Institute of Pathogenesis and Disease Prevention, Shinshu University Graduate School of Medicine, Matsumoto, Japan
Jia Huo
Department of Orthopedic Surgery, the Third Hospital of Hebei Medical University, Shijiazhuang, China
Hiroki Miyahara
Department of Neuro-health Innovation, Institute for Biomedical Sciences, Interdisciplinary Cluster for Cutting Edge Research, Shinshu University, Matsumoto, Japan; Department of Aging Biology, Shinshu University School of Medicine, Matsumoto, Japan
Masayuki Mori
Department of Neuro-health Innovation, Institute for Biomedical Sciences, Interdisciplinary Cluster for Cutting Edge Research, Shinshu University, Matsumoto, Japan; Department of Aging Biology, Shinshu University School of Medicine, Matsumoto, Japan
Keiichi Higuchi
Department of Neuro-health Innovation, Institute for Biomedical Sciences, Interdisciplinary Cluster for Cutting Edge Research, Shinshu University, Matsumoto, Japan; Department of Aging Biology, Shinshu University School of Medicine, Matsumoto, Japan
Curcumin is a polyphenol compound that exhibits multiple physiological activities. To elucidate the mechanisms by which curcumin affects systemic amyloidosis, we investigated amyloid deposition and molecular changes in a mouse model of amyloid apolipoprotein A-II (AApoAII) amyloidosis, in which mice were fed a curcumin-supplemented diet. Curcumin supplementation for 12 weeks significantly increased AApoAII amyloid deposition relative to controls, especially in the liver and spleen. Liver weights and plasma ApoA-II and high-density lipoprotein concentrations were significantly elevated in curcumin-supplemented groups. RNA-sequence analysis revealed that curcumin intake affected hepatic lipid metabolism via the peroxisome proliferator-activated receptor (PPAR) pathway, especially PPARα activation, resulting in increased Apoa2 mRNA expression. The increase in liver weights was due to activation of PPARα and peroxisome proliferation. Taken together, these results demonstrate that curcumin is a PPARα activator and may affect expression levels of proteins involved in amyloid deposition to influence amyloidosis and metabolism in a complex manner.
