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PI3K/AKT/GLUT1
RSC Advances · 2018 ·Vol. 8 ·期 43 ·24470-24476 · IF 2.936

Apigenin ameliorates vascular injury in rats with high fructose-induced metabolic disturbance by inhibiting PI3K/AKT/GLUT1

Xiaofang Chen,Jianyang Tan,Lu Zhang,Yonggang Liu,Yahong Cheng,Qianying Zhang,Hong Ding

The abuse of fructose in daily diet may cause cardiovascular diseases that seriously threaten human health, and both safe and efficient solutions need to be developed. We investigated whether apigenin can prevent the harmful impact of excessive fructose on cardiovascular events. Based on the reduction of percentage of body fat and systolic pressure as well as the improvements in insulin resistance, lipid metabolism, and pathological injury to the thoracic aorta, we suggested that high levels of fructose cause vascular injury and metabolic disorders, which can be improved to some extent by using apigenin. Fundamentally, apigenin down-regulates levels of phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), and glucose transporter 1 (GLUT1), which increase with high concentrations of fructose. Moreover, the inflammation and asymmetric dimethylarginine (ADMA) levels increased in fructose group, but they decreased when the rats were fed with apigenin. The results suggest that PI3K/AKT/GLUT1 may have potential for alleviating cardiovascular injury, and apigenin can be an excellent candidate for supplements to ameliorate cardiovascular diseases related to high fructose consumption.

CAS / MDL: 57-48-7
研究领域: 药理学 · 心血管疾病 · 代谢 · 营养学
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