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目的 :探讨肝十二指肠韧带内注射利多卡因减轻肝脏缺血 再灌注 (Ischemia reprefusion ,I R)损伤的有效性以及从蛋白质组水平研究其可能涉及的机制。方法 :4 6只SD大鼠随机分成I R组、利多卡因组和开腹组。检测各组血清丙氨酸转氨酶 (ALT)和门冬氨酸转氨酶 (AST) ,肝脏组织标本胎盘蓝染色分析。肝脏组织的蛋白质组学分析采用双向聚丙烯酰胺凝胶电泳 (2 DPAGE)、质谱 (MALDI TOF MS)方法。结果 :利多卡因组ALT和AST较I R组显著降低 (ALT :t=2 .5 99,P <0 .0 2 ;AST :t=2 .992 ,P <0 .0 1) ,胎盘蓝染色的无活性肝细胞较I R组也明显减少。利多卡因组的 2 DPAGE图谱较I R组发生了改变 ,质谱鉴定出 11个差异表达的蛋白质 ,其中 6个上调表达 ,5个下调表达。结论 :肝十二指肠韧带内注射利多卡因预处理有效地减轻了大鼠肝脏随后的I R损伤 ,是一种保护面临I R损伤肝脏的新方法。蛋白质组学研究可见 ,利多卡因预处理改变了肝脏I R后的蛋白质表达。
Objective: To investigate the efficacy of lidocaine injection in hepaticoduodenal ligament to reduce the damage of hepatic ischemia-reperfusion injury (I R) and to investigate its possible mechanism from the proteome level. Methods: Forty-six SD rats were randomly divided into I R group, lidocaine group and laparotomy group. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and placental staining of liver tissue were detected. Proteomic analysis of liver tissues was performed by two-dimensional polyacrylamide gel electrophoresis (2 DPAGE) and mass spectrometry (MALDI TOF MS). Results: The ALT and AST in the lidocaine group were significantly lower than those in the IR group (ALT: t = 2.559, P <0. 02; AST: t = 2.992, P <0.01) Of inactive hepatocytes also significantly reduced compared with IR group. The 2-DPAGE pattern of lidocaine group was changed compared with that of I R group. Eleven differentially expressed proteins were identified by mass spectrometry, of which 6 were up-regulated and 5 were down-regulated. CONCLUSION: Pretreatment with lidocaine in the hepatoduodenal ligament effectively reduces the subsequent I R injury in rat livers, and is a new method to protect the liver from I R injury. Proteomics studies showed that lidocaine pretreatment altered protein expression after I R in the liver.