首页> 外文期刊>BioMed research international >Partial Portal Vein Arterialization Attenuates Acute Bile Duct Injury Induced by Hepatic Dearterialization in a Rat Model
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Partial Portal Vein Arterialization Attenuates Acute Bile Duct Injury Induced by Hepatic Dearterialization in a Rat Model

机译:部分门静脉动脉化衰减了大鼠模型中肝脏肝癌诱导的急性胆管损伤

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Hepatic infarcts or abscesses occur after hepatic artery interruption. We explored the mechanisms of hepatic deprivation-induced acute liver injury and determine whether partial portal vein arterialization attenuated this injury in rats. Male Sprague-Dawley rats underwent either complete hepatic arterial deprivation or partial portal vein arterialization, or both. Hepatic ischemia was evaluated using biochemical analysis, light microscopy, and transmission electron microscopy. Hepatic ATP levels, the expression of hypoxia- and inflammation-associated genes and proteins, and the expression of bile transporter genes were assessed. Complete dearterialization of the liver induced acute liver injury, as evidenced by the histological changes, significantly increased serum biochemical markers, decreased ATP content, increased expression of hypoxia- and inflammation-associated genes and proteins, and decreased expression of bile transporter genes. These detrimental changes were extenuated but not fully reversed by partial portal vein arterialization, which also attenuated ductular reaction and fibrosis in completely dearterialized rat livers. Collectively, complete hepatic deprivation causes severe liver injury, including bile infarcts and biloma formation. Partial portal vein arterialization seems to protect against acute ischemia-hypoxia-induced liver injury.
机译:肝动脉中断后发生肝梗塞或脓肿。我们探讨了肝脏剥夺诱导的急性肝损伤的机制,并确定部分门静脉动脉化是否降低了大鼠损伤。雄性Sprague-Dawley大鼠完成完全肝动脉剥夺或部分门静脉动脉化,或两者。使用生物化学分析,光学显微镜和透射电子显微镜评估肝缺血。肝脏ATP水平,评估缺氧和炎症相关基因和蛋白质的表达,以及胆汁转运蛋白的表达。完全肝脏诱导急性肝损伤的亲人化,如组织学变化所证明,显着增加的血清生化标志物,降低的ATP含量,缺氧和炎症相关基因和蛋白质的表达增加,并降低了胆汁转运蛋白基因的表达。这些有害的变化令人不安但不完全通过部分门静脉动脉化完全逆转,这也是在完全亲人化的大鼠肝脏中衰减的导管反应和纤维化。集体,完全肝脏剥夺导致严重的肝损伤,包括胆汁梗塞和毕赤瘤形成。部分门静脉动脉化似乎可以防止急性缺血缺氧诱导的肝损伤。

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