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首页> 外文期刊>Lipids in Health Disease >Dietary saponins of sea cucumber alleviate orotic acid-induced fatty liver in rats via PPARα and SREBP-1c signaling
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Dietary saponins of sea cucumber alleviate orotic acid-induced fatty liver in rats via PPARα and SREBP-1c signaling

机译:日粮海参皂苷通过PPARα和SREBP-1c信号传导减轻大鼠乳清酸诱导的脂肪肝

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Background Nonalcoholic fatty liver disease is the most common chronic liver disease in the world, and is becoming increasingly prevalent. Saponins of sea cucumber (SSC) are proven to exhibit various biological activities. Therefore, the present study was undertaken to examine the effect of saponins extracted from sea cucumber (Pearsonothuria graeffei) on the preventive activity of fatty liver in rats. Methods Male Wistar rats were randomly divided into five groups, including normal control group, fatty liver model group, SSC-treated group with SSC at levels of 0.01%, 0.03% and 0.05%. Model rats were established by administration with 1% orotic acid (OA). After the experiment period, serum total cholesterol (TC), triglyceride (TG), and hepatic lipid concentrations were determined. To search for a possible mechanism, we examined the changes of key enzymes and transcriptional factors involved in hepatic lipids biosynthesis, fatty acid β-oxidation. Results Both 0.03% and 0.05% SSC treatment alleviated hepatic steatosis and reduced serum TG and TC concentration significantly in OA fed rats. Hepatic lipogenic enzymes, such as fatty acid synthase (FAS), malic enzyme (ME), and glucose-6-phosphate dehydrogenase (G6PDH) activities were inhibited by SSC treatment. SSC also decreased the gene expression of FAS, ME, G6PDH and sterol-regulatory element binding protein (SREBP-1c). Otherwise, the rats feeding with SSC showed increased carnitine palmitoyl transferase (CPT) activity in the liver. Hepatic peroxisome proliferator-activated receptor (PPARα), together with its target gene CPT and acyl-CoA oxidase (ACO) mRNA expression were also upregulated by SSC. Conclusions According to our study, the lipids-lowering effect of dietary SSC may be partly associated with the enhancement of β-oxidation via PPARα activation. In addition, the inhibited SREBP-1c- mediated lipogenesis caused by SSC may also contribute to alleviating fatty liver.
机译:背景技术非酒精性脂肪肝是世界上最常见的慢性肝病,并且正变得越来越普遍。事实证明,海参皂苷(SSC)具有多种生物活性。因此,本研究旨在研究从海参中提取的皂苷(Pearsonothuria graeffei)对大鼠脂肪肝的预防作用。方法将雄性Wistar大鼠随机分为5组,分别为正常对照组,脂肪肝模型组,SSC治疗组,SSC水平分别为0.01%,0.03%和0.05%。通过施用1%乳清酸(OA)建立模型大鼠。实验期过后,测定血清总胆固醇(TC),甘油三酸酯(TG)和肝脂质浓度。为了寻找可能的机制,我们检查了涉及肝脂质生物合成,脂肪酸β-氧化的关键酶和转录因子的变化。结果0.03%和0.05%SSC处理均可减轻OA喂养大鼠的肝脂肪变性并显着降低血清TG和TC浓度。 SSC处理可抑制肝脂肪酶,例如脂肪酸合酶(FAS),苹果酸酶(ME)和葡萄糖-6-磷酸脱氢酶(G6PDH)活性。 SSC还降低了FAS,ME,G6PDH和固醇调节元件结合蛋白(SREBP-1c)的基因表达。否则,喂食SSC的大鼠肝脏中的肉碱棕榈酰转移酶(CPT)活性增加。肝过氧化物酶体增殖物激活受体(PPARα)及其靶基因CPT和酰基辅酶A氧化酶(ACO)mRNA表达也被SSC上调。结论根据我们的研究,饮食中SSC的降脂作用可能部分与PPARα活化引起的β-氧化作用增强有关。此外,由SSC引起的SREBP-1c介导的脂肪生成抑制也可能有助于减轻脂肪肝。

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