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薏苡仁油通过抑制 p-AMPK/SePP1/apoER2 通路的激活减轻非酒精性脂肪性肝病中的脂肪堆积。

Coix lacryma-jobi Seed Oil Reduces Fat Accumulation in Nonalcoholic Fatty Liver Disease by Inhibiting the Activation of the p-AMPK/SePP1/apoER2 Pathway.

机构信息

Shandong University of Traditional Chinese Medicine.

Shandong Provincial Chinese Medicine Classical Prescription Demonstration Engineering Technology Research Center.

出版信息

J Oleo Sci. 2021 May 1;70(5):685-696. doi: 10.5650/jos.ess20255. Epub 2021 Apr 12.

Abstract

The lipid metabolism disorder is the key role of Nonalcoholic fatty liver disease (NAFLD). Selenoprotein P plays an important role in the pathological process of lipid accumulation. Coix lacryma-jboi seed oil (CLSO) is an active component extracted from Coix lacryma-jobi seed (CLS) which has been found to be effective of reducing blood fat and antioxidative. But the effect and mechanism of CLSO on NAFLD are not clear. The aim of this study was to explore the therapeutic effect and mechanism of CLSO in the treatment of NAFLD. Our result showed that CLSO decreased the liver/body weight ratio, lowered the total cholesterol (TC) and triacylglycerol (TG), and elevated the high density lipoprotein (HDL) in serum. CLSO reduced the lipid deposition in the liver of NAFLD rats. In addition, CLSO could bring down the abnormal expression of superoxide dismutase (SOD) and malondialdehyde (MDA). Moreover, CLSO significantly declined the liver apolipoprotein E (apoE), apolipoprotein E receptor (apoER) and selenoprotein P 1 (SePP1) expression. In vivo, CLSO decreased the lipid droplets and TG level, reduced the protein expression of SePP1, apoER, phosphor-adenosine 5'-monophosphate (AMP)-activated protein kinase (p-AMPK) in the cytoplasm of HepG2 cells induced by oleic acid and palmitic acid (OP). At the same time, lipid accumulation was observed in the Sepp1 high expression cells induced by endoplasmic reticulum (ER) activator tunicamycin (Tm). CLSO could identically reduce the protein expression of SePP1, apoER, p-AMPK in the cytoplasm of HepG2 cells induced by Tm. This result not only proved the CLSO had therapeutic effect on NAFLD, but also confirmed its mechanism associated with degrading the phosphorylation of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) which led to the decrease of the expression SePP1/apoER2 in order to reduce lipid accumulation. The study suggests CLSO has great medicinal value in treating NAFLD besides its edibility.

摘要

脂质代谢紊乱是非酒精性脂肪性肝病(NAFLD)的关键作用。硒蛋白 P 在脂质积累的病理过程中发挥重要作用。薏苡仁油(CLSO)是从薏苡仁(CLS)中提取的一种活性成分,已被发现具有降低血脂和抗氧化作用。但 CLSO 对 NAFLD 的作用及机制尚不清楚。本研究旨在探讨 CLSO 治疗 NAFLD 的疗效及机制。我们的结果表明,CLSO 降低了肝/体重比,降低了总胆固醇(TC)和三酰甘油(TG),提高了血清中的高密度脂蛋白(HDL)。CLSO 减少了 NAFLD 大鼠肝脏中的脂质沉积。此外,CLSO 可以降低超氧化物歧化酶(SOD)和丙二醛(MDA)的异常表达。此外,CLSO 显著降低了肝脏载脂蛋白 E(apoE)、载脂蛋白 E 受体(apoER)和硒蛋白 P1(SePP1)的表达。在体内,CLSO 降低了油酸和棕榈酸(OP)诱导的 HepG2 细胞中的脂滴和 TG 水平,降低了 SePP1、apoER、磷酸腺苷 5'-单磷酸(AMP)激活蛋白激酶(p-AMPK)的蛋白表达。同时,内质网(ER)激活剂衣霉素(Tm)诱导的 Sepp1 高表达细胞中观察到脂质堆积。CLSO 可同样降低 Tm 诱导的 HepG2 细胞胞质中 SePP1、apoER、p-AMPK 的蛋白表达。这一结果不仅证明了 CLSO 对 NAFLD 有治疗作用,而且证实了其机制与降低磷酸化腺苷 5'-单磷酸(AMP)激活蛋白激酶(AMPK)的磷酸化有关,从而导致 SePP1/apoER2 的表达降低,从而减少脂质堆积。该研究表明,CLSO 除了具有食用价值外,在治疗 NAFLD 方面具有很大的药用价值。

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