Calycosin directly improves perivascular adipose tissue dysfunction by upregulating the adiponectin/AMPK/eNOS pathway in obese mice,Food & Function

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Calycosin directly improves perivascular adipose tissue dysfunction by upregulating the adiponectin/AMPK/eNOS pathway in obese mice
Food & Function ( IF 5.1 ) Pub Date : 2018-03-27 00:00:00 , DOI: 10.1039/c8fo00328a
Fang Han _{1,

2,

3,

4} , Kai Li _{2,

3,

4,

5} , Ruiyan Pan _{3,

4,

6,

7} , Wenjie Xu _{2,

3,

4,

8} , Xue Han _{2,

3,

4,

8} , Ningning Hou _{2,

3,

4,

8} , Xiaodong Sun _{2,

3,

4,

8}

Affiliation

Perivascular adipose tissue (PVAT) loses its anti-contractile activity in obesity. Calycosin, the major bioactive isoflavonoid, was shown to protect endothelial function. However, effects of calycosin on PVAT function in obesity remain unclear. We aimed to investigate the effects of calycosin on the anti-contractile activity of PVAT in obese mice and its potential mechanisms. Obesity in mice was induced with a high-fat diet, with or without calycosin treatment. Thoracic aorta responses to phenylephrine were determined. AMP protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS) levels were analyzed by western blotting. Adiponectin, TNF-α levels and superoxide production were measured in the PVAT. Calycosin treatment significantly increased the anti-contractile response of PVAT, which was impaired in obese mice. This beneficial effect of calycosin was eliminated by treatments of blocking adiponectin, AMPK or eNOS. Similar results were observed for calycosin treatment ex vivo. Treatment of obese mice with calycosin significantly increased adiponectin levels, activated AMPK and eNOS phosphorylation and reduced superoxide production and TNF-α levels in PVAT. Our results indicated that calycosin restored PVAT induced anti-contractile activity and affected PVAT function through the adiponectin/AMPK/eNOS pathway in obese mice.

中文翻译：

Calycosin通过上调肥胖小鼠的脂联素/ AMPK / eNOS途径直接改善血管周围脂肪组织功能障碍

在肥胖症中，血管周围脂肪组织（PVAT）失去其抗收缩活性。Calycosin是主要的生物活性异黄酮，可保护内皮功能。然而，在肥胖症中，calycosin对PVAT功能的作用尚不清楚。我们旨在研究calycosin对肥胖小鼠PVAT的抗收缩活性的影响及其潜在机制。高脂饮食可导致小鼠肥胖，无论是否进行钙黏蛋白治疗。确定了胸主动脉对去氧肾上腺素的反应。通过蛋白质印迹分析了AMP蛋白激酶（AMPK）和内皮型一氧化氮合酶（eNOS）的水平。在PVAT中测量脂联素，TNF-α水平和超氧化物的产生。Calycosin处理显着增加了PVAT的抗收缩反应，这在肥胖小鼠中受损。通过阻断脂联素，AMPK或eNOS的治疗，消除了calycosin的这种有益作用。钙黏蛋白治疗的结果相似离体。用calycosin治疗肥胖小鼠可显着增加脂联素水平，激活AMPK和eNOS磷酸化并降低PVAT中的超氧化物生成和TNF-α水平。我们的结果表明，在肥胖小鼠中，calycosin通过脂联素/ AMPK / eNOS途径恢复了PVAT诱导的抗收缩活性并影响了PVAT功能。

更新日期：2018-03-27

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