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Curcumin promotes AApoAII amyloidosis and peroxisome proliferation in mice by activating the PPAR? signaling pathway.


ABSTRACT: 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 PPAR? activation, resulting in increased Apoa2 mRNA expression. The increase in liver weights was due to activation of PPAR? and peroxisome proliferation. Taken together, these results demonstrate that curcumin is a PPAR? activator and may affect expression levels of proteins involved in amyloid deposition to influence amyloidosis and metabolism in a complex manner.

SUBMITTER: Dai J 

PROVIDER: S-EPMC7880682 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

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Curcumin promotes AApoAII amyloidosis and peroxisome proliferation in mice by activating the PPARα signaling pathway.

Dai Jian J   Li Ying Y   Kametani Fuyuki F   Cui Xiaoran X   Igarashi Yuichi Y   Huo Jia J   Miyahara Hiroki H   Mori Masayuki M   Higuchi Keiichi K  

eLife 20210126


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  ...[more]

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