CAJ | 학술논문

目的观察缺血后处理可以减轻大鼠肾缺血再灌注损伤(IPI)后肾小管间质纤维化的作用及其机制.方法建立原位大鼠单侧肾缺血再灌注动物模型,摘除右肾后对左肾行缺血后处理,即10s再灌注,10 s缺血,6次循环后再灌注12周.实验动物分为缺血再灌注损伤组(IRI),缺血后处理组(IPO)和假手术组(Sham),全自动生化分析仪检测血尿素氮(BUN)和肌酐(Cr),Masson特殊染色法观察小管间质纤维化程度；Western blotin法测定α平滑肌肌动蛋白(α-SMA)、转化生长因子(TGF-β)和磷酸化Smad2蛋白表达(p-Smad2)；免疫组织化学法观察肾脏α-SMA和TGF-β1的分布.结果 IRI组和IPO组较Sham组出现了明显肾间质纤维化,但是IPO组肾间质纤维化与IRI组比较有所减轻；α-SMA、TGF-β1和p-Smad2的水平明显减低,各组间差异有统计学意义(P＜0.05).结论肾脏缺血再灌注损伤可以引起小管间质纤维化.缺血后处理可以影响此病理改变,其保护机制可能为缺血后处理抑制TGF-β1和p-Smad2信号通路激活.
목적 관찰결혈후처리가이감경대서신결혈재관주손상(IPI)후신소관간질섬유화적작용급기궤제.방법 건립원위대서단측신결혈재관주동물모형,적제우신후대좌신행결혈후처리,즉10s재관주,10 s결혈,6차순배후재관주12주.실험동물분위결혈재관주손상조(IRI),결혈후처리조(IPO)화가수술조(Sham),전자동생화분석의검측혈뇨소담(BUN)화기항(Cr),Masson특수염색법관찰소관간질섬유화정도；Western blotin법측정α평활기기동단백(α-SMA)、전화생장인자(TGF-β)화린산화Smad2단백표체(p-Smad2)；면역조직화학법관찰신장α-SMA화TGF-β1적분포.결과 IRI조화IPO조교Sham조출현료명현신간질섬유화,단시IPO조신간질섬유화여IRI조비교유소감경；α-SMA、TGF-β1화p-Smad2적수평명현감저,각조간차이유통계학의의(P＜0.05).결론 신장결혈재관주손상가이인기소관간질섬유화.결혈후처리가이영향차병리개변,기보호궤제가능위결혈후처리억제TGF-β1화p-Smad2신호통로격활.
Objectives In the present study,we investigated whether ischemic postconditioning effects on the development of tubulointerstitial fibrosis follow renal I/R injury.Methods Rat models of warm renal I/R were established by clamping left pedicles for 45 minutes after right nephrectomy,both with and without treatment with ischemic postconditioning,and then reperfused for up to 12 weeks.Serum urea nitrogen and creatinine levels,expression of proteinα-SMA 、TGF-β1 和1 p-Smad2 were compared after renal injury.HE and Massongtrichrome staining were used to assess renal fibrosis.Results Our data showed that ischemic postconditioning attenuated the level of tubulointerstitial fibrosis after 12 weeks.Ischemic postconditioning also inhibited the protein expression ofα-SMA 、TGF-β1 和 p-Smad2.Conclusions The results indicated that ischemic postconditioning has beneficial effects on renal fibrosis.Its mechanisms may involve inhibition of the TGF-βl/Smad pathway to exert protective effects.