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Hepatoprotective effect of coffee pulp aqueous extract combined with simvastatin against hepatic steatosis in high-fat diet-induced obese rats

机译:咖啡浆含水提取物联合辛伐他汀对高脂饮食诱导肥胖大鼠肝硬化的肝脏保护作用

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摘要

This study investigated the effect of coffee pulp aqueous extract (CPE) on obesity- induced hepatic steatosis in rats and the mechanism involved. Male Wistar rats were fed high-fat diet for 12 weeks and supplemented with 1000 mg/kg BW CPE or 40 mg/kg BW simvastatin or CPE combined with 20 mg/kg BW simvastatin for another 12 weeks. The lipid profiles, presence of insulin resistance, development of hepatic steatosis and related mechanisms were investigated. Results show that CPE, simvastatin and combined treatment improved lipid profiles, insulin resistance, oxidative stress and hepatic steatosis. Correspondingly, CPE induced the lipolytic gene PPAR alpha, while combination treatment additively suppressed the lipogenic genes PPAR gamma and SREBP1-c. Such effects downregulated the fatty acid transporter FAT/CD36, and activated AMPK, which concomitantly improved obese induced-hepatic steatosis. Collectively, hepato-protective effects of CPE, particularly combined with simvastatin, could broaden the therapeutic options for hyperlipidaemia and NAFLD patients who receive lipid-lowering drugs.
机译:本研究研究了咖啡浆含水提取物(CPE)对大鼠肥胖诱导的肝脏脂肪变性的影响和所涉及的机制。雄性Wistar大鼠喂食高脂饮食12周,并补充1000mg / kg BW CPE或40 mg / kg BW Simvastatin或CPE与20mg / kg BW Simvastatin合并另外12周。研究了脂质曲线,胰岛素抵抗的存在,肝脏脂肪变性的发展和相关机制。结果表明,CPE,辛伐他汀和组合治疗改善了脂质曲线,胰岛素抵抗,氧化应激和肝脏脂肪变性。相应地,CPE诱导脂肪溶解基因PPARα,而组合治疗加剧抑制了脂质基因PPARγ和Srebp1-C。这些效果下调了脂肪酸转运脂/ CD36,并激活的AMPK,其伴随地改善了肥胖诱导的肝脏脂肪变性。共同地,CPE的肝保护作用,特别联合辛伐他汀,可以扩大接受降脂药物的高脂血症和NAFLD患者的治疗选择。

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