Metabolic syndrome (MetS) is an increasing health threat and often leads to cardiovascular complications. The aim of this study was to evaluate icariin’s ability to combat MetS induced in rats and outline the involved mechanisms of action. Rats were grouped in four batches. The controls received a regular diet and water. MetS was induced in the remaining three groups using a high-salt high-fructose diet. Groups 1 and 2 were given daily doses of saline, while Groups 3 and 4 received 25 and 50 mg/kg icariin, respectively, for 12 weeks in total. The experimental protocol was carried out for 12 weeks consecutively. Icariin significantly decreased body mass index (BMI), adiposity index and body weight. Further, icariin protected against dyslipidemia, hyperglycemia, and hyperinsulinemia and improved insulin resistance as given by the homeostatic model assessment of insulin resistance (HOMA-IR) values. Icariin guarded against the rise in serum interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α). In addition, it significantly inhibited the decrease in mRNA expression of glucose transporter type 4 (GLUT4) and liver kinase B1 (LKB1). These effects were accompanied by decreased liver content of nuclear factor kappa B (NFκB) and enhanced serum levels of phosphorylated 5ʹ-adenosine monophosphate-activated protein kinase (p-AMPK). Further, icariin significantly increased p-AMPK/AMPK ratio in liver tissues. Conclusively, icariin offers protection in experimentally induced MetS, partially due to AMPK activation.

代谢综合症（MetS）对健康的威胁越来越大，经常导致心血管并发症。这项研究的目的是评估icariin对抗大鼠诱发的MetS的能力并概述其参与的作用机制。将大鼠分为四批。对照组接受常规饮食和水。在其余三组中，使用高盐高果糖饮食诱导了MetS。第1组和第2组每天接受盐水注射，而第3组和第4组分别分别接受25和50 mg / kg大麻素，共12周。实验方案连续进行了12周。鹰嘴豆素显着降低了体重指数（BMI），肥胖指数和体重。此外，icariin可防止血脂异常，高血糖，胰岛素抵抗的稳态模型评估（HOMA-IR）值可得出高胰岛素血症和改善的胰岛素抵抗。伊卡瑞林可防止血清白介素6（IL-6）和肿瘤坏死因子α（TNF-α）升高。此外，它显着抑制4型葡萄糖转运蛋白（GLUT4）和肝激酶B1（LKB1）mRNA表达的下降。这些作用伴随着核因子κB（NFκB）肝脏含量的减少和磷酸化5ʹ-腺苷单磷酸激活蛋白激酶（p-AMPK）的血清水平升高。此外，柠檬酸显着增加肝组织中的p-AMPK / AMPK比率。结论是，icariin部分地由于AMPK激活而在实验诱导的MetS中提供保护。伊卡瑞林可防止血清白介素6（IL-6）和肿瘤坏死因子α（TNF-α）升高。此外，它显着抑制4型葡萄糖转运蛋白（GLUT4）和肝激酶B1（LKB1）mRNA表达的下降。这些作用伴随着肝细胞核因子κB（NFκB）含量的降低和血清磷酸化5'-腺苷单磷酸激活蛋白激酶（p-AMPK）含量的升高。此外，柠檬酸显着增加肝组织中的p-AMPK / AMPK比率。结论是，icariin部分地由于AMPK激活而在实验诱导的MetS中提供保护。伊卡瑞林可防止血清白介素6（IL-6）和肿瘤坏死因子α（TNF-α）升高。此外，它显着抑制4型葡萄糖转运蛋白（GLUT4）和肝激酶B1（LKB1）mRNA表达的下降。这些作用伴随着核因子κB（NFκB）肝脏含量的减少和磷酸化5ʹ-腺苷单磷酸激活蛋白激酶（p-AMPK）的血清水平升高。此外，柠檬酸显着增加肝组织中的p-AMPK / AMPK比率。结论是，icariin部分地由于AMPK激活而在实验诱导的MetS中提供保护。这些作用伴随着核因子κB（NFκB）肝脏含量的减少和磷酸化5ʹ-腺苷单磷酸激活蛋白激酶（p-AMPK）的血清水平升高。此外，柠檬酸显着增加肝组织中的p-AMPK / AMPK比率。结论是，icariin部分由于AMPK激活而在实验诱导的MetS中提供保护。这些作用伴随着核因子κB（NFκB）肝脏含量的减少和磷酸化5ʹ-腺苷单磷酸激活蛋白激酶（p-AMPK）的血清水平升高。此外，柠檬酸显着增加肝组织中的p-AMPK / AMPK比率。结论是，icariin部分地由于AMPK激活而在实验诱导的MetS中提供保护。