TZDs reduce mitochondrial ROS production and enhance mitochondrial biogenesis

被引：73

作者：

Fujisawa, Kazuo ^{[1
]}

Nishikawa, Takeshi ^{[1
]}

Kukidome, Daisuke ^{[1
]}

Imoto, Koujirou ^{[1
]}

Yamashiro, Takeshi ^{[1
]}

Motoshima, Hiroyuki ^{[1
]}

Matsumura, Takeshi ^{[1
]}

Araki, Eiichi ^{[1
]}

机构：

[1] Kumamoto Univ, Dept Metab Med, Fac Med & Pharmaceut Sci, Kumamoto 8608556, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2009年 / 379卷 / 01期

关键词：

Diabetes; Diabetic complications; Reactive oxygen species; Mitochondria; Thiazolidinediones (TZDs); PPAR gamma coactivator-1 alpha (PGC-1 alpha); INTENSIVE INSULIN THERAPY; OXIDATIVE STRESS; PIOGLITAZONE; EXPRESSION; PREVENTS; COMPLICATIONS; GLIMEPIRIDE; DYSFUNCTION; PROGRESSION; APOPTOSIS;

D O I：

10.1016/j.bbrc.2008.11.141

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Although it has been reported that thiazolidinediones (TZDs) may reduce cardiovascular events in type 2 diabetic patients, its precise mechanism is unclear. We previously demonstrated that hyperglycemia-induced production of reactive oxygen species from mitochondria (mtROS) contributed to the development of diabetic complications, and metformin normalized mt ROS production by induction of MnSOD and promotion of mitochondrial biogenesis by activating the PGC-1 alpha pathway. In this study, we examined whether TZDs could inhibit hyperglycemia-induced mtROS production by activating the PGC-1 alpha. pathway. We revealed that pioglitazone and ciglitazone attenuated hyperglycemia-induced ROS production in human umbilical vein endothelial cells (HUVECs). Both TZDs increased the expression of NRF-1, TFAM and MnSOD mRNA. Moreover, pioglitazone increased mtDNA and mitochondrial density. These results suggest that TZDs normalize hyperglycemia-induced mtROS production by induction of MnSOD and promotion of mitochondrial biogenesis by activating PGC-1 alpha. This phenomenon could contribute to the prevention of diabetic vascular complications. (C) 2008 Elsevier Inc. All rights reserved.

引用

页码：43 / 48

页数：6

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