アカギリ　サトミ   Akagiri Satomi   赤桐　里美    所属   医学研究科 医学研究科 (医学部医学科をご参照ください)    職種   特任助教
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Astaxanthin protects mesangial cells from hyperglycemia-induced oxidative signaling.
掲載誌名	正式名：Journal of cellular biochemistry 略　 称：J Cell Biochem ISSNコード：10974644/07302312
掲載区分	国外
巻・号・頁	103(6),pp.1925-1937
著者・共著者	Manabe Emiko, Handa Osamu, Naito Yuji, Mizushima Katsura, Akagiri Satomi, Adachi Satoko, Takagi Tomohisa, Kokura Satoshi, Maoka Takashi, Yoshikawa Toshikazu
発行年月	2008/04/15
概要	Astaxanthin (ASX) is a carotenoid that has potent protective effects on diabetic nephropathy in mice model of type 2 diabetes. In this study, we investigated the protective mechanism of ASX on the progression of diabetic nephropathy using an in vitro model of hyperglycemia, focusing on mesangial cells. Normal human mesangial cells (NHMCs) were cultured in the medium containing normal (5 mM) or high (25 mM) concentrations of D-glucose. Reactive oxygen species (ROS) production, the activation of nuclear transcription factors such as nuclear factor kappa B (NFkappaB) and activator protein-1 (AP-1), and the expression/production of transforming growth factor-beta 1 (TGFbeta(1)) and monocyte chemoattractant protein-1 (MCP-1) were evaluated in the presence or absence of ASX. High glucose (HG) exposure induced significant ROS production in mitochondria of NHMCs, which resulted in the activation of transcription factors, and subsequent expression/production of cytokines that plays an important role in the mesangial expansion, an important event in the pathogenesis of diabetic nephropathy. ASX significantly suppressed HG-induced ROS production, the activation of transcription factors, and cytokine expression/production by NHMCs. In addition, ASX accumulated in the mitochondria of NHMCs and reduced the production of ROS-modified proteins in mitochondria. ASX may prevent the progression of diabetic nephropathy mainly through ROS scavenging effect in mitochondria of mesangial cells and thus is expected to be very useful for the prevention of diabetic nephropathy.
DOI	10.1002/jcb.21583
PMID	17955498