Long-term baicalin administration ameliorates metabolic disorders and hepatic steatosis in rats given a high-fat diet

Long-term baicalin administration ameliorates metabolic disorders and hepatic steatosis in rats given a high-fat diet
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长期服用黄芩苷可改善高脂饮食大鼠的代谢紊乱和肝脂肪变性

DOI:
10.1038/aps.2009.150
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发表时间:
2009-11-01
影响因子:
8.2
通讯作者:
Peng, Hong-li
Peng, Hong-li
中科院分区:
医学1区
文献类型:
--
作者:
Guo, Hong-xia;Liu, Dai-hua;Peng, Hong-li

文献摘要

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目的:黄芩苷是黄芩中的主要黄酮类化合物之一,具有抗氧化和抗炎作用。然而,黄芩苷对代谢紊乱和肝脂肪变性的影响还没有被investigated.Methods:在高脂饮食(HFD)喂养的大鼠或没有黄芩苷治疗的体重进行了检查。在实验结束时,分析血清生化参数、肝组织学和脂质谱,以评估动物是否患有代谢紊乱或肝脂肪变性。在肝脏中,AMP激活的蛋白激酶(AMPK)和乙酰辅酶A羧化酶(ACC)的磷酸化和参与脂肪生成的一些酶的基因表达进行了检查。黄芩苷对高糖诱导的人肝癌HepG2细胞AMPK磷酸化和脂质蓄积的影响也进行了检查。结果:黄芩苷(80 mg/kg)ip给药16周可抑制HFD喂养大鼠的体重增加。体重减轻伴随着内脏脂肪量的减少。黄芩苷显著降低高脂饮食引起的血清胆固醇、游离脂肪酸和胰岛素浓度升高。黄芩苷还通过降低血清肿瘤坏死因子α水平抑制全身炎症反应。黄芩苷减少肝脏脂质蓄积,增强AMPK和ACC的磷酸化,下调脂肪生成相关基因,包括脂肪酸合成酶及其上游调控因子SREBP-1c。结论:黄芩苷可能通过抑制AMPK磷酸化而抑制脂肪肝及肥胖相关疾病的发生发展。
Aim:Baicalin, one of the major flavonoids in Scutellaria baicalensis, possesses antioxidant and anti-inflammatory properties. However, the effects of baicalin on metabolic disorders and hepatic steatosis have not been investigated.Methods:Body weight was examined in high-fat diet (HFD)-fed rats with or without baicalin treatment. At the end of the experiment, serum biochemical parameters, liver histology and lipid profile were analyzed to assess whether the animals were suffering from metabolic disorders or hepatic steatosis. In the liver, the phosphorylation of AMP activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) and the gene expression of some enzymes involved in lipogenesis were examined. The effects of baicalin on the phosphorylation of AMPK and lipid accumulation induced by high glucose in human hepatoma HepG2 cells were also examined.Results:Baicalin (80 mg/kg) administered ip for 16 weeks suppressed body weight gain in HFD-fed rats. Weight reduction was accompanied by the reduction of visceral fat mass. Baicalin significantly decreased the elevated serum cholesterol, free fatty acid and insulin concentrations caused by the HFD. Baicalin also suppressed systemic inflammation by reducing the serum level of tumor necrosis factor α. Baicalin reduced hepatic lipid accumulation, enhanced the phosphorylation of AMPK and ACC and down-regulated genes involved in lipogenesis, including fatty acid synthase and its upstream regulator SREBP-1c. In HepG2 cells, baicalin (5 and 10 μmol/L) increased the phosphorylation of AMPK and decreased lipid accumulation following the addition of high glucose.Conclusion:Our study suggests that baicalin might have beneficial effects on the development of hepatic steatosis and obesity-related disorders by targeting the hepatic AMPK.