肾缺血后处理通过抑制p38 MAPK信号通路减轻大鼠肾缺血再灌注损伤

Renal ischemia postconditioning can alleviate renal ischemia reperfusion injury in rats by inhibiting p38 MAPK signaling pathway

目的:探讨肾缺血后处理通过抑制p38 MAPK信号通路对大鼠肾缺血再灌注损伤的影响。方法:采用中线剖腹手术和右肾切除术,将大鼠随机分为3组:假手术组(sham)、肾缺血再灌注组(I/R)和肾脏缺血后处理组(RI-Post)进行后续实验,全自动生化分析仪检测肾功能指标,HE染色观察肾组织损伤情况,TUNEL染色和免疫组化检测caspase-3的表达,试剂盒检测氧化应激指标,Western blot检测p38 MAPK表达。结果:I/R组肾损伤情况及肾小管损伤评分高于RI-Post组与sham组,肾缺血后处理较肾缺血后灌注可以明显降低肾组织的损伤程度,肾缺血后处理可以降低肾缺血后再灌注氧化应激水平,I/R组促进p38 MAPK信号通路表达,而RI-Post组可能通过抑制p38 MAPK信号通路表达降低肾组织损伤。结论:肾缺血后处理通过抑制p38 MAPK信号通路减轻大鼠肾缺血再灌注损伤程度。

Objective:To investigate the effect of renal ischemia post-processing on renal ischemia reperfusion injury in rats by inhibiting p38 MAPK signaling pathway.Methods:The rats were randomly divided into 3 groups by midline laparotomy and right nephrectomy.The follow-up experiments were conducted in the sham surgery group,the renal ischemical reperfusion group(I/R)and the renal ischemic postconditioning group(RI-Post).Automatic biochemical analyzer was used to detect renal function indexes,HE staining was used to observe renal tissue damage,TUNEL staining and immunohistochemistry were used to detect Caspase-3 expression,oxidative stress indexes were detected with the kit,and p38 MAPK expression was detected with the Western blot.Results:The renal injury and renal tubule injury scores in I/R group were higher than those in RI-Post group and sham group.Compared with renal ischemia reperfusion,renal ischemia postprocessing could significantly reduce the degree of renal tissue injury,renal ischemia postprocessing could reduce the level of oxidative stress after renal ischemia reperfusion,and I/R group could promote the expression of p38 MAPK signaling pathway.However,in the RI-Post group,renal tissue injury might be reduced by inhibiting the expression of p38 MAPK signaling pathway.Conclusion:Renal ischemia post-processing can reduce the severity of renal ischemia reperfusion injury in rats by inhibiting p38 MAPK signaling pathway.