首页> 外文期刊>Archives of Biological Sciences >Protective effects of pumpkin (Cucurbita pepo L.) seed oil on rat liver damage induced by chronic alcohol consumption
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Protective effects of pumpkin (Cucurbita pepo L.) seed oil on rat liver damage induced by chronic alcohol consumption

机译:南瓜(CuCurbita Pepo L.)种子油对慢性饮酒消费诱导大鼠肝损伤的保护作用

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Pumpkin seed oil (PSO) possesses a protective potential against liver injury due to the presence of biologically active ingredients. Adult male albino rats were administrated PSO (per os, 2 mL/kg b.w./day) and a 12% ethanol solution in water, ad libitum, with an average intake of 8.14 g of ethanol/kg bw/day for 6 weeks. Congestion, hepatic central vein dilation, portal vein branch dilation, Kupffer cell hyperplasia, fatty liver changes, hepatocyte focal necrosis were observed after daily alcohol intake. All observed changes were reduced when PSO was ingested with ethanol. PSO intake itself induced discrete cellular edema, congestion and slight dilatation of the central and portal vain branches. Chronic ethanol intake elevated catalase (CAT) activity and glutathione reductase (GR) protein expression; concomitant PSO intake had no effect on CAT activity or GR protein expression. PSO intake decreased the activities of GR, glutathione-S-transferase (GST) and xanthine oxidase (XOD) in the liver, probably due to the ingestion of antioxidants. Intake of PSO and ethanol significantly decreased cytosolic superoxide dismutase (SOD1) and increased NF-κB protein expression compared to ethanol intake, suggesting that the protective effects of PSO were mediated by the NF-κB signaling pathway. Our results reveal a therapeutic potential of PSO in alcoholic liver disease.
机译:由于存在生物活性成分,南瓜种子油(PSO)具有免受肝损伤的保护潜力。将成年雄性白化大鼠施用PSO(每对OS,2mL / kg B.W./Day)和12%的水,AD Libitum乙醇溶液,平均摄入量为8.14g乙醇/ kg bw /天6周。肝脏中央静脉扩张,门静脉分支扩张,Kupffer细胞增生,脂肪肝脏变化,每日酒精摄入后观察到肝细胞局灶性坏死。当用乙醇摄取PSO时,所有观察到的变化都会降低。 PSO进气本身诱导离散的细胞水肿,挤塞和距离中央和门户网站的轻微扩张。慢性乙醇进气升高过氧化氢酶(猫)活性和谷胱甘肽还原酶(GR)蛋白表达;伴随PSO摄入对猫活性或GR蛋白表达没有影响。 PSO进气量降低了肝脏中GR,谷胱甘肽-S-转移酶(GST)和黄嘌呤氧化酶(XOD)的活性,可能是由于抗氧化剂的摄取。与乙醇摄入相比,胞质超氧化物歧化酶(SOD1)和NF-κB蛋白表达增加显着降低了PSO和乙醇,表明PSO的保护作用是由NF-κB信号传导途径介导的。我们的结果揭示了PSO在酒精性肝病中的治疗潜力。

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