Beneficial effect of 7-O-galloyl-d-sedoheptulose on oxidative stress and hepatic and renal changes in type 2 diabetic db/db mice
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- 作者：Chan Hum Park ; Jeong Sook Noh ; Noriko Yamabe ; Ki Sung Kang ; Takashi Tanaka ; Takako Yokozawa
- 关键词：7-O-Galloyl-d-sedoheptulose ; db/db mice ; Advanced glycation endproduct ; Abnormal lipid metabolism ; Inflammation ; Liver ; Kidney
- 刊名：European Journal of Pharmacology
- 出版年：2010
- 出版时间：25 August 2010
- 年：2010
- 卷：640
- 期：1-3
- 页码：233-242
- 全文大小：1084 K
文摘
The aim of the present study was to evaluate the beneficial effects of 7-O-galloyl-d-sedoheptulose (GS), isolated from Corni Fructus, on hepatic and renal lipid metabolisms and advanced glycation endproduct formation followed by oxidative stress and inflammation using type 2 diabetic mice. GS was orally administered to db/db mice at doses of 20 and 100 mg/kg body weight per day for 8 weeks, and its effects were compared with those of the vehicle in db/db and m/m mice. The serum, hepatic, and renal biochemical factors, and protein expressions related to lipid metabolism, inflammation, advanced glycation endproducts, and their receptors, were measured. After 8 weeks of GS treatment, elevation of serum adiponectin as well as an improvement of hepatic and renal functional parameters was shown in db/db mice, and significant reductions of lipids in serum, liver, and kidney were observed according to the down-regulation of sterol regulatory element-binding protein-1. Moreover, GS inhibited oxidative stress and advanced glycation endproduct formation and their receptor expressions in the liver and kidney of db/db mice. These results suggest that GS could effectively inhibit advanced glycation endproduct formation caused by oxidative stress and/or dyslipidemia in the liver and kidney of db/db mice. Furthermore, the augmented expression of nuclear factor-kappa B p65 and its related inflammatory protein expressions were down-regulated in GS-treated groups. In conclusion, GS could have hepato- and reno-protective effects against abnormal lipid metabolism and the reactive oxygen species-related formation of advanced glycation endproducts with inflammation in type 2 diabetes.