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作 者:扈红蕾 高健 郭文君[2] 周风华[2] 刘红燕 宿长春 HU Hong-Lei;GAO Jian;GUO Wen-Jun;ZHOU Feng-Hua;LIU Hong-Yan;SU Chang-Chun(Weifang School of Nursing Vocational College Weifang Campus,Weifang 261041,China;Department of Pathology,Weifang Medical College,Weifang 261042,China)
机构地区:[1]潍坊护理职业学院潍坊校区,潍坊261041 [2]潍坊医学院病理学教研室,潍坊261042
出 处:《生理学报》2019年第5期725-731,共7页Acta Physiologica Sinica
基 金:supported by a Scientific Program from the Weifang City Health Bureau,Shandong Province,China(No.2014129)
摘 要:本文旨在研究富氢水在黄曲霉毒素B1 (aflatoxin B1, AFB1)致大鼠急性肝损伤模型中的抗损伤作用及保护机制。将健康雄性Sprague-Dawley (SD)大鼠随机分为对照组、模型组(AFB1组)和富氢水处理组(AFB1+H2组),采用单次灌胃AFB1 (2.0 mg/kg)建立大鼠急性AFB1肝损伤模型,并给予富氢水灌胃干预。用HE染色观察肝组织病理变化,下腔静脉取血检测血清肝功能指标,取肝组织检测丙二醛(malonaldehyde, MDA)和还原型谷胱甘肽(glutathione, GSH)含量,用Western blot检测MAPK信号通路蛋白(ERK、JNK和p38 MAPK)磷酸化水平。结果显示,相对AFB1组,AFB1+H2组大鼠体重增加,AFB1引起的急性肝损伤显著减轻,血清谷丙转氨酶、谷草转氨酶活性和总胆红素含量降低,肝组织中MDA含量降低,还原型GSH含量升高,肝组织ERK、JNK、p38 MAPK磷酸化水平显著下调。上述结果提示,富氢水可减轻AFB1肝损伤,其机制可能与富氢水减轻AFB1引起的氧化应激、抑制MAPK信号转导通路的激活有关。The purpose of this study was to investigate the anti-injury effect and protective mechanism of hydrogen-enriched water in a rat model of acute liver injury induced by aflatoxin B1(AFB1). Healthy male Sprague-Dawley(SD) rats were randomly divided into control group, model group(AFB1 group) and hydrogen-enriched water treatment group(AFB1+H2 group). The rat model of acute liver injury induced by AFB1 was established by single intragastric administration of AFB1(2.0 mg/kg), and then the rats were treated with hydrogen-enriched water intragastrically. HE staining was used to observe the pathological changes of liver tissue. Blood samples were taken from vena cava to measure serum liver function indexes. Live tissue was sampled to detect malondialdehyde(MDA) and reduced glutathione(GSH) contents. Western blot was used to detect phosphorylation levels of MAPK signaling pathway proteins(ERK, JNK and p38 MAPK). The results showed that, compared with the AFB1 group, the AFB1+H2 group exhibited increased body weights, alleviated acute liver injury, decreased activities of serum glutamic-pyruvic transaminase and glutamic oxaloacetic transaminase, as well as total bilirubin level in the serum. Meanwhile, hydrogen-enriched water decreased MDA content and increased GSH content in liver tissue. AFB1-increased phosphorylation levels of ERK, JNK and p38 MAPK in liver tissue were down-regulated significantly by hydrogen-enriched water treatment. These results suggest that hydrogen-enriched water can alleviate liver injury induced by AFB1, and its mechanism may be related to the reduction of oxidative stress and the inhibition of MAPK signal transduction pathway activation.
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