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題名 | Role of Hepatic Nitric Oxide Synthases in Rats with Thioacetamide-induced Acute Liver Failure and Encephalopathy=肝內氧化氮合成酶分型於Thioacetamide引發之急性肝衰竭及肝腦病變中所扮演的角色 |
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作者姓名(中文) | 黃惠君; 王聖賢; 陳祖裕; 陳億周; 李發耀; 張扶陽; 朱啟仁; 林漢傑; 盧瑞華; 李壽東; | 書刊名 | 中華醫學會雜誌 |
卷期 | 70:1 2007.01[民96.01] |
頁次 | 頁16-23+CA3 |
分類號 | 415.53 |
關鍵詞 | 猛爆性肝衰竭; 肝腦病變; 氧化氮; 氧化氮合成酶; Fulminant hepatic failure; Hepatic encephalopathy; Nitric oxide; Nitric oxide synthase; Thioacetamide; |
語文 | 英文(English) |
中文摘要 | 背景:肝腦病變,是一種續發於肝臟代償不全或肝門一系統血管異常交通之神經精神方面的異常狀態。過去研究顯示,抑制氧化氮合成,會使由thioacetamide (TAA)引發急性肝衰竭老鼠之肝腦病變惡化,並提高死亡率,顯示氧化氮可能扮演了一個保護性的角色。此研究探討血管內皮生成之固有型氧化氮合成及誘發型氧化氮合成,於猛爆性肝衰竭合併肝腦病病之大鼠肝內所扮演的角色。 方法:雄性大白鼠(300—350g) 隨機接受三天之腹腔內注射TAA(每天每公斤350毫克)一生理食鹽水。之後以Opto-Varimex animal activity meter 評估嚴重度,並抽血測定血中alanine aminotransferase (ALT),aspartate aminotranfsferase (AST),alkaline phosphatase,及bilirubin的濃度。此外,肝臟中固有及誘發型氧化氮合成的RNA及蛋白質的表現,亦分別以reverse transcription—polynerease chain reaction及Western blot進行分析。 結果:TAA組之活動性護計數較生理食鹽組低。肝內固有型氧化氮合成而非誘發型氧化氮合成之mRNA及蛋白質表現,於TAA組則則顯著曾強。此外,肝內固有型氧化氮合成之mRNA的表現強度與總活動量計數成反比,但是ALT及AST的指數成正比。肝內固有型氧化氮合成之蛋白質的表現,亦與ALT,AST及bilirubin的然數成正比。 結論:肝內固有型氧化氮合成之表現,於TAA引發大鼠的猛爆性肝衰竭及肝腦病病後有增強的現象,這或許扮演了一種調控的角色。 |
英文摘要 | Background: Hepatic encephalopathy is neuropsychiatric derangement secondary to hepatic decompensation or portal-systemic shunting. Nitric oxide (NO) synthase inhibition aggravates encephalopathy and increases mortality in rats with thioacetamide (TAA)-induced acute liver failure, suggesting a protective role of NO. This study investigated the roles of endothelium-derived constitutive NO synthase (eNOS) and inducible NOS (iNOS) in the liver of rats with fulminant hepatic failure and encephalopathy. Methods: Male Sprague-Dawley rats (300–350 g) were randomized to receive TAA 350 mg/kg/day, by intraperitoneal injection or normal saline for 3 days. Severity of encephalopathy was assessed with the Opto-Varimex animal activity meter. Plasma levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, and bilirubin were measured. Hepatic iNOS and eNOS RNA and protein expressions were assessed by reverse transcription–polymerase chain reaction and Western blot analyses, respectively. Results: The TAA group showed lower motor activity counts than the normal saline group. Hepatic eNOS, but not iNOS, mRNA and protein expressions were enhanced in the TAA group. In addition, hepatic eNOS mRNA expression was negatively correlated with total movement but positively correlated with ALT and AST. Protein expression of hepatic eNOS was positively correlated with ALT, AST and bilirubin. Conclusion: Upregulation of hepatic eNOS was observed in rats with TAA-induced fulminant hepatic failure and encephalopathy, which might play a regulatory role. |
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