Reperfusion But Not Ischemia Induces the Expression of Inducible Nitric Oxide Synthase in Rat Liver

缺血後再灌流是刺激鼠肝表現誘發型一氧化氮合成酶之主要因素

陳昭富(Chao-Fuh Chen) ； 呂福江(Furr-Jlang Leu) ； 汪大衛(David Wang) ； 蔣桂芳(Kuei-Fang Chiang) ； 陳幸一(Hsing-I Chen)

《臺灣消化醫學雜誌》 22卷1期 (2005/03) Pp. 1-9

https://doi.org/10.6557/GJT.200503_22(1).0001

摘要

This study was designed to analyze the expression of inducible nitric oxide synthase (iNOS) in a rat model of ischemia and ischemia/reperfusion (I/R)-induced liver injury. Real-tune polymerase chain reaction and immunohistochemistry were used to observe the mRNA and protein expression of iNOS. Ischemia was induced by clamping the common hepatic artery and portal vein of rats for 40 min. Thereafter; flow was restored, and the liver was reperfused for 90 min. Blood samples collected prior to ischemia, immediately post-ischemia and 90 min after reperfusion were analyzed for hydroxyl radical and nitric oxide (NO) levels. Blood levels of aspartate transferase (AST), alanine transferase (ALT) and lactate dehydrogenase (LDH), which served as indices of liver injury, were also measured. This protocol resulted in elevation of the blood NO (p＜0.01), hydroxyl radical (p＜0.001), ASI ALT and LDH (p＜0.001) in the I/R hut not in the ischemia group or sham-operated group. The mRNA expression of iNOS was increased 25.7±5.6-fold, and protein expression of iNOS was increased 22.4±1.8-fold in liver tissue after I/R but not after ischemia alone. The difference in liver injury between ischemia and I/R could he explained by the significantly higher nitrotyrosine expression (27.2±3.3-fold increase) in liver tissue in the I/R group than in the ischemia group, indicating that the oxygen radical and nitric oxide reaction product, peroxynitrite, acting to nitrate protein, might play a critical role in I/R-induced liver injury.

關鍵字

一氧化氮合成酶表現 ； 缺血 ； 再灌流 ； 肝

並列摘要

This study was designed to analyze the expression of inducible nitric oxide synthase (iNOS) in a rat model of ischemia and ischemia/reperfusion (I/R)-induced liver injury. Real-tune polymerase chain reaction and immunohistochemistry were used to observe the mRNA and protein expression of iNOS. Ischemia was induced by clamping the common hepatic artery and portal vein of rats for 40 min. Thereafter; flow was restored, and the liver was reperfused for 90 min. Blood samples collected prior to ischemia, immediately post-ischemia and 90 min after reperfusion were analyzed for hydroxyl radical and nitric oxide (NO) levels. Blood levels of aspartate transferase (AST), alanine transferase (ALT) and lactate dehydrogenase (LDH), which served as indices of liver injury, were also measured. This protocol resulted in elevation of the blood NO (p＜0.01), hydroxyl radical (p＜0.001), ASI ALT and LDH (p＜0.001) in the I/R hut not in the ischemia group or sham-operated group. The mRNA expression of iNOS was increased 25.7±5.6-fold, and protein expression of iNOS was increased 22.4±1.8-fold in liver tissue after I/R but not after ischemia alone. The difference in liver injury between ischemia and I/R could he explained by the significantly higher nitrotyrosine expression (27.2±3.3-fold increase) in liver tissue in the I/R group than in the ischemia group, indicating that the oxygen radical and nitric oxide reaction product, peroxynitrite, acting to nitrate protein, might play a critical role in I/R-induced liver injury.

並列關鍵字

iNOS expression ； ischemia ； reperfusion ； liver