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目的:探讨p38MAPK、MMP-2在大鼠肾缺血再灌注后早期的表达情况及其在肾缺血再灌注损伤中的作用。方法:选择健康雄性SD大鼠48只,随机分成假手术(sham)组24只,缺血再灌注(IR)组24只,建立大鼠肾缺血再灌注损伤模型,测定各组实验大鼠血清肌酐水平的变化,应用免疫组织化学二步法检测p38MAPK、MMP-2表达的变化。结果:与sham组比较,IR组血清肌酐水平升高,缺血45分钟再灌注24小时达高峰(P<0.01)。MMP-2蛋白在sham组呈少量散在表达或不表达,缺血45分钟再灌注6小时有少量表达,再灌注12小时、24小时及72小时呈阳性表达,以24小时达高峰(P<0.05);p38MAPK蛋白在sham组呈少量散在表达或不表达,缺血45分钟再灌注6小时、12小时及24小时呈阳性表达,12小时达高峰(P<0.05)。p38MAPK、MMP-2蛋白的表达与血清肌酐水平的变化呈显著正相关。结论:肾缺血再灌注可激活p38MAPK,活化的p38MAPK可以上调MMP-2蛋白的表达,可能促进了肾缺血再灌注损伤的发生和发展。
OBJECTIVE: To investigate the expression of p38MAPK and MMP-2 in early stage after renal ischemia-reperfusion in rats and its role in renal ischemia-reperfusion injury. Methods: Forty-eight healthy male Sprague-Dawley rats were randomly divided into sham group (24 rats) and ischemia-reperfusion group (24 rats). Rat renal ischemia-reperfusion injury model was established. Serum creatinine levels were detected by immunohistochemical two-step detection of p38MAPK, MMP-2 expression changes. Results: Compared with sham group, serum creatinine level increased in IR group and peaked at 24 hours after ischemia for 45 minutes (P <0.01). The expression of MMP-2 protein was little or no expression in sham group. The expression of MMP-2 protein was slight in 6 hours after reperfusion for 45 minutes and 12 hours, 24 hours and 72 hours after reperfusion, reaching the peak at 24 hours (P <0.05 ). The p38MAPK protein was scattered or not expressed in the sham group at a dose of 6 hours after reperfusion for 45 minutes and reached the peak at 12 and 24 hours (P <0.05). The expressions of p38MAPK and MMP-2 were positively correlated with the changes of serum creatinine. CONCLUSION: Renal ischemia-reperfusion can activate p38MAPK. Activation of p38MAPK up-regulates the expression of MMP-2 protein and may promote the occurrence and development of renal ischemia-reperfusion injury.