【摘要】 目的观察肝缺血再灌注和缺血预处理后ERK1/2活化的情况,以探讨其在肝脏缺血再灌注损伤和缺血预处理保护中的作用。方法120只Wistar大鼠随机分成缺血再灌注组(IR),缺血预处理组(IP)与假手术组(SO组),利用肝原位部分缺血再灌注模型,于复灌后0、0.5、1、2、4、8、12和24h取材,应用免疫组织化学的方法对磷酸化的p-ERK1/2进行免疫组化检测并作半定量分析,观察其在缺血再灌注损伤和缺血预处理中的变化。结果p-ERK在缺血后即有轻度地增高,但在再灌注后30min开始增高明显,持续到再灌注后4h,高峰出现在再灌注后2h。与IR组相比,IP组p-ERK的表达在再灌注后1、2和4h较IR组增高(P<0.05)。结论缺血预处理可通过增高ERK1/2的磷酸化水平,减轻缺血再灌注导致的肝脏损伤,ERK1/2通路可能在缺血预处理的保护作用中起重要的作用。更多还原

【Abstract】 [Objective] To Study activation of ERK1/2 in hepatic ischemia-reperfusion and hepatic ischemic preconditioning settings, and its role in hepatic ischemia-reperfusion injury and protection in hepatic preconditioning. [Methods] The orthotopic partial hepatic ischemia/reperfusion animal model was used. 120 Wistar rats were randomly divided into ischemia/reperfusion (IP) group, ischemic preconditioning (IP) group and sham operation (SO) group. Liver tissue was harvested at 0, 0.5, 1, 2, 4, 8, 12, 24 h after ischemia/reperfusion in both IP and IR groups. The phosphorylated ERK1/2 (p-ERK1/2) was detected by immunohistochemistry and half-quantitative analysis was made to study its expression changes in IR and IP settings. [Results] p-ERK1/2 increased slightly after ischemia and increased significantly at 30 minutes after reperfusion in IR group and IP group, the high level was kept to 4 hours after reperfusion, its peak time occurred at 2 hours after reperfusion. Compared with IR group, the expression of p-ERK in IP group was significantly higher at 1-, 2- and 4 hours after reperfusion (P <0.05). [Conclusion] Ischemic preconditioning can increase the phosphorylation levels of ERK, which can attenuate ischemia-reperfusion injury of the rat liver. These results suggest that ERK1/2 pathway may play a vital role in ischemic preconditioning.更多还原