The protective role of Kangen‐karyu against fructose‐induced metabolic syndrome in a rat model

The protective role of Kangen‐karyu against fructose‐induced metabolic syndrome in a rat model
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Kangen-karyu 对大鼠模型中果糖诱导的代谢综合征的保护作用

DOI:
10.1211/jpp.59.9.0012
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发表时间:
2007
影响因子:
3.3
通讯作者:
Eun
Eun
中科院分区:
医学3区
文献类型:
--
作者:
T. Yokozawa;H. J. Kim;N. Yamabe;T. Okamoto;Eun

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使用大鼠模型研究了还原核提取物的保护作用及其对果糖诱导的代谢综合征的机制。雄性 Wistar 大鼠被喂食高果糖 (65%) 饮食或标准食物一周,并在随后的两周内用 50 或 100 mg kg−1 体重/天的 Kangen-karyu 提取物或载体进行治疗。与正常大鼠相比,高果糖喂养大鼠的血清葡萄糖、糖基化蛋白、甘油三酯(TG)、总胆固醇和血压水平升高。然而,Kangen-karyu 提取物可改善高果糖诱导的代谢综合征,包括高血糖和高甘油三酯血症。此外,Kangen-karyu 提取物对甾醇调节元件结合蛋白 (SREBP)-1 表达的调节显着抑制了高果糖饮食大鼠肝脏 TG 含量的增加。另一方面,过氧化物酶体增殖物激活受体 α 和 SREBP-2 蛋白水平不受高果糖饮食或 Kangen-karyu 提取物喂养的影响。此外,对高果糖喂养的大鼠施用还原核提取物显着降低了血清、肝匀浆和线粒体中硫代巴比妥酸反应物质的水平。此外,它通过调节肝脏中的核因子-κB (NF-κB) 和 bcl-2 蛋白来抑制环氧合酶 (COX)-2 的增加,这表明 Kangenkaryu 提取物对代谢综合征的保护潜力可能归因于 COX-2、NF-κB 和 bcl-2 信号通路的调节。本研究表明,Kangen-karyu 提取物通过调节肝脏 SREBP-1 蛋白和 NF-κB 信号通路,降低 TG 和胆固醇含量,显着改善高果糖诱导的代谢综合征,如高血糖、高脂血症和高血压。
The protective effect of Kangen‐karyu extract and its mechanisms against fructose‐induced metabolic syndrome have been investigated using a rat model. Male Wistar rats were fed a high fructose (65%) diet or standard chow for one week, and for two subsequent weeks were treated with 50 or 100 mg kg−1 body weight/day Kangen‐karyu extract or vehicle. Serum glucose, glycosylated protein, triglyceride (TG), total cholesterol, and blood pressure levels of high‐fructose‐fed rats were increased compared with those of normal rats. However, Kangen‐karyu extract ameliorated the high‐fructose‐induced metabolic syndrome including hyperglycaemia and hypertriglyceridaemia. In addition, the increase of hepatic TG content in rats given the high fructose diet was significantly inhibited with the regulation of sterol regulatory element‐binding protein (SREBP)‐1 expression by Kangen‐karyu extract. On the other hand, peroxisome proliferator‐activated receptor α and SREBP‐2 protein levels were not affected by the feeding of the high fructose diet or Kangen‐karyu extract. Moreover, Kangen‐karyu extract administration to high‐fructose‐fed rats markedly reduced the thiobarbituric acid‐reactive substance levels in serum, hepatic homogenate, and mitochondria. Furthermore, it inhibited the increase of cyclooxygenase (COX)‐2 with the regulation of nuclear factor‐kappa B (NF‐κB) and bcl‐2 proteins in the liver, suggesting that the protective potential of Kangenkaryu extract against metabolic syndrome would be attributed to the regulation of COX‐2, NF‐κB, and bcl‐2 signalling pathways. This study indicated that Kangen‐karyu extract significantly improved high‐fructose‐induced metabolic syndrome such as hyperglycaemia, hyperlipidaemia, and hypertension through the reductions of TG and cholesterol contents with the regulation of hepatic SREBP‐1 protein and the NF‐κB signalling pathway.
DOI: 10.1124/mol.53.1.14
发表时间: 1998-01-01
影响因子: 3.6
作者:
Palmer, CNA;Hsu, MH;Johnson, EF
通讯作者: Johnson, EF