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富硒麦芽对实验性肝癌大鼠NO、NOS和脂质过氧化的影响 被引量:4

Influence of Selenium-enriched Malt on Nitric Oxide,Nitric Oxide Synthase,Lipid Peroxidation in Hepatoma Rats
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摘要 50只清洁级SD大鼠随机分为4组:对照组(5只)、模型组(15只)、富硒麦芽组(15只)和亚硒酸钠组(15只)。对照组和模型组饲喂大鼠基础饲料,饲料含硒量为0.1mg/kg;富硒麦芽组和亚硒酸钠组分别在基础饲料中补充富硒麦芽和亚硒酸钠,饲料含硒量为3.0mg/kg。除对照组外,其余3组采用0.01%二乙基亚硝胺(DEN)诱发大鼠肝癌16周,停止诱癌后继续饲养2周再处死全部大鼠,观察富硒麦芽对丙氨酸氨基转移酶(ALT)、碱性磷酸酶(ALP)、白蛋白(ALB)、总胆红素(TBIL)、一氧化氮(NO)、一氧化氮合成酶(NOS)、丙二醛(MDA)和谷胱甘肽过氧化物酶(GSH-Px)的影响。结果显示,富硒麦芽组大鼠血浆ALT、ALP、TBIL、NO、MDA和肝组织NO、NOS、MDA显著低于模型组,全血和肝组织GSH-Px活性显著高于模型组;与亚硒酸钠组相比,富硒麦芽组大鼠血浆和肝组织的NO含量和NOS活性显著降低。试验表明富硒麦芽具有减轻肝脏损伤、延缓大鼠肝癌形成的能力,其作用机制之一可能为富硒麦芽能抑制NO的产生,清除体内大量过剩的氧自由基,减轻NO等自由基所致的脂质过氧化损伤。 Fifty SD rats were allotted to four groups randomly,which were subjected to the following treatments:feeding with the basal diet containing 0.1 mg/kg selenium as control group in: 5) and model group(n=15);supplementation with selenium-enriched malt and sodium selenite to the basal diet at a final concentration of 3.0 mg/kg selenium as selenium-enriched malt group(n= 15) and sodium selenite group(n= 15),at the same time,hepatoma was induced by drinking with 0.01% diethylnitrosamine(DEN) in rats of model group,selenium-enriched malt group and sodium selenite group for 16 weeks. After another two weeks,the rats were killed and effects of selenium-enriched malt on alanine amiotransterase (ALT),alkaline phosphatase (ALP), albumin (ALB), total bilirubln ( TBIL ) in plasma and nitric oxide (NO), nitric oxide synthase ( NOS ), malondialdehyde (MDA) and glutathione-peroxidase(GSH-Px) in plasma and liver tissue were examined. The results indicated that plasma ALT ,AI.P ,TBIL ,NO,MDA and NO,MDA,NOS of liver tissue in the selenium-enriched malt group were significantly lower than those in the model group,the GSH-Px in plasma and liver tissue were significantly higher than those of the model group ;Comparing with the sodium selenite group,NO and NOS in plasma and liver tissue in the selenium-enriched malt group were significantly decreased. It was demonstrated that selenium-enriched malt could attenuate the lesion of liver cells and delay the development of hepatoma induced by DEN. One of the mechanisms might be to restrain the produce of NO,eliminate excessive oxide free radicals and alleviate lipid peroxidation lesion induced by NO and other free radicals.
出处 《中国兽医学报》 CAS CSCD 北大核心 2006年第6期681-683,共3页 Chinese Journal of Veterinary Science
基金 教育部高校博士点基金资助项目(20020307022) 江苏省"九五"农业攻关项目(BE98301) 国家"十五"科技攻关项目(2002BA574A10-1-6)
关键词 富硒麦芽 大鼠肝癌 NO NOS 脂质过氧化 selenium-enriched malt rat hepatocarcinogenesis nitric oxide nitric oxide synthase lipid peroxidation Corresponding author
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