首页> 外文期刊>RSC Advances >Patchouli oil isolated from the leaves of Pogostemon cablin ameliorates ethanol-induced acute liver injury in rats via inhibition of oxidative stress and lipid accumulation
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Patchouli oil isolated from the leaves of Pogostemon cablin ameliorates ethanol-induced acute liver injury in rats via inhibition of oxidative stress and lipid accumulation

机译:从Pogostemon cablin叶片中分离出的广香油可通过抑制氧化应激和脂质蓄积来改善乙醇诱发的大鼠急性肝损伤

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Excessive alcohol consumption can cause serious hepatic injury which is associated with oxidative stress and fatty metabolic disturbance. Patchouli oil (PO) is a sort of food supplement with high medicinal value in hepatoprotection, but its ability against ethanol-induced liver failure has not been demonstrated. Thus, this study aimed to investigate the potential hepatoprotection of PO through an ethanol-induced hepatotoxicity rat model. Our results showed that PO pretreatment could dramatically decrease the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) in serum, paralleled by an improvement of histopathology alterations. Additionally, PO could markedly suppress the content of reactive oxygen species (ROS), tumor necrosis factor alpha (TNF-α), free fatty acid (FFA), and triglyceride (TG), while enhancing the activities of glutathione (GSH), glutathione reductase (GR), and superoxide dismutase (SOD) as well as the ratio of glutathione to oxidized glutathione (GSH/GSSG) in liver. The protective effect of PO against oxidative stress was interrelated with restraining the mRNA and protein expression of hepatic microsomal enzyme cytochrome P450 2E1 (CYP2E1). What's more, PO pretreatment could also accelerate lipometabolism via up-regulating expressions of adenosine monophosphate-activated protein kinase (AMPK), peroxisome proliferator-activated receptor α (PPAR-α), and carnitine palmitoyltransferase 1 (CPT-1) and down-regulating expressions of nuclear factor-kappaB (NF-κB) p65, sterol regulatory element-binding protein 1 (SREBP-1c), fatty acid synthase (FAS), and stearoyl-CoA desaturase 1 (SCD-1). To conclude, PO showed potent effect against ethanol-induced hepatotoxicity by relieving oxidative stress and preventing lipid accumulation.
机译:过量饮酒会导致严重的肝损伤,这与氧化应激和脂肪代谢紊乱有关。广香油(PO)是一种具有高药用价值的食品保肝剂,但其抗乙醇性肝功能衰竭的能力尚未得到证实。因此,本研究旨在通过乙醇诱导的大鼠肝毒性模型研究PO的潜在肝保护作用。我们的结果表明,PO预处理可以显着降低血清中丙氨酸转氨酶(ALT),天冬氨酸转氨酶(AST),碱性磷酸酶(ALP)和乳酸脱氢酶(LDH)的水平,同时改善组织病理学改变。此外,PO可以显着抑制活性氧(ROS),肿瘤坏死因子α(TNF-α),游离脂肪酸(FFA)和甘油三酸酯(TG)的含量,同时增强谷胱甘肽(GSH),谷胱甘肽的活性还原酶(GR)和超氧化物歧化酶(SOD)以及肝脏中谷胱甘肽与氧化型谷胱甘肽的比例(GSH / GSSG)。 PO对氧化应激的保护作用与抑制肝微粒体酶细胞色素P450 2E1(CYP2E1)的mRNA和蛋白表达有关。而且,PO预处理还可以通过上调腺苷单磷酸激活的蛋白激酶(AMPK),过氧化物酶体增殖物激活的受体α(PPAR-α)和肉碱棕榈酰转移酶1(CPT-1)的表达来加速脂肪代谢。核因子-κB(NF-κB)p65,固醇调节元件结合蛋白1(SREBP-1c),脂肪酸合酶(FAS)和硬脂酰-CoA去饱和酶1(SCD-1)的表达。总而言之,PO通过减轻氧化应激和防止脂质堆积,对乙醇诱导的肝毒性表现出有效的作用。

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