NLRP3炎性反应小体在缺血再灌注急性肾损伤大鼠肾组织中的表达研究

NLRP3 inflammatory corpuscle in ischemia reperfusion of acute kidney injury in the rat kidney expression research

目的:研究NLRP3炎性反应小体在缺血再灌注急性肾损伤大鼠肾组织中的表达。方法:选取SD雄性大鼠14只,平均分为缺血再灌注组(A组)和假手术组(B组),对比两组之间血肌酐、尿素氮变化及NLRP3表达的差异情况。结果:A组大鼠血肌酐、尿素氮水平明显高于B组大鼠,差异有统计学意义(P<0.05);免疫组化显示缺血再灌注急性肾损伤组大鼠肾小管上皮细胞NLRP3的表达显著增强;病理学检查显示缺血再灌注组大鼠肾小管间质损伤较严重。结论:缺血再灌注急性肾损伤会伴随血肌酐水平升高以及肾组织NLRP3表达增强。

Objective To study the NLRP3 inflammatory corpuscle in ischemia-reperfusion expression in acute kidney injury in the rat kidney. Method 14 only selection methods: SD male rats, divided into ischemia reperfusion group (group A) and control group (group B), the contrast between the two groups of changes in serum creatinine,blood urea nitrogen and NLRP3 expression differences. Results The group A rat serum creatinine, blood urea nitrogen level obviously were higher than that of group B in the rat, there difference was statistically significant (P <0. 05);Immunohistochemical display of ischemia reperfusion group with the acute kidney injury rat renal tubular epithelial cells the expression of NLRP3 significantly enhanced;Pathological examination showed ischemia reperfusion group rat renal tubular interstitial damage more serious. Conclusion Ischemia reperfusion of acute kidney injury is associated with elevated serum creatinine levels and renal tissue NLRP3 expression enhancement.