摘要
目的探讨缺血后处理对梗阻性黄疸肾缺血再灌注损伤大鼠血清TNF-α水平的影响。方法 60只SD大鼠随机分成梗阻性黄疸对照组(S组)、梗阻性黄疸肾缺血再灌注组(I/R组)、梗阻性黄疸肾缺血再灌注缺血后处理组(IPO组),每组20只。根据缺血后再灌注时间点各组又分为再灌注0 h(T0)、1 h(T1)、3 h(T2)、6 h(T3)4个亚组各5例。检测再灌注后的各时点血清中尿素氮(BUN)、肌酐(Cr)、TNF-α水平,观察肾组织的病理改变。结果 I/R组和IPO组血清BUN、Cr、TNF-α水平均高于S组(P均<0.05),IPO组T2时间点血清Cr、BUN、TNF-α水平均低于I/R组(P均<0.05)。结论缺血后处理可以下调大鼠血清TNF-α水平,从而减轻梗阻性黄疸大鼠肾缺血再灌注损伤,其机制可能与抑制炎症反应有关。
Objective To investigate effect of ischemic postconditioning on kidney ischemia-reperfusion injury and the expression of TNF-α in obstructive jaundice rats. Methods Totally 60 SD rats were randomly divided into three groups( n= 20) : obstructive jaundice group( group S),obstructive jaundice renal Ischemia-reperfusion group( group I / R),obstructive jaundice + ischemic postconditioning group( group IPO). According to the time of ischemia reperfusion,each group was divided into four subgroups( n = 5) : 0 h reperfusion( T0),1 h reperfusion( T1),3 h reperfusion( T2),6 h reperfusion( T3). In each period,the serum urea of nitrogen( BUN),creatinine( Cr) and TNF-α were collected and observed,kidney pathological changes were observed. Results Compared with group S,the serum levels of BUN and Cr increased,TNF-α in renal tissue were upregulated in groups I / R and IPO( all P < 0. 05). At T2,compared with group I/R,the serum levels of BUN,Cr and TNF-α decreased( all P < 0. 05). Conclusions Ischemic postconditioning can downregulate the expression of TNF-α and alleviate the renal ischemia-reperfusion injury in obstructive jaundice rats,whith may be through inhibiting inflammatory reactions.
出处
《山东医药》
CAS
北大核心
2015年第5期25-27,共3页
Shandong Medical Journal
基金
珠海市科研计划基金项目(2014D0401990018)
关键词
梗阻性黄疸
缺血后处理
缺血再灌注损伤
肾脏
肿瘤坏死因子-α
大鼠
ischemic postconditioning
ischemia reperfusion injury
kidney
obstructive jaundice
tumor necrosis factor-α
rats
