山东医药
山東醫藥
산동의약
SHANDONG MEDICAL JOURNAL
2015年
5期
25-27
,共3页
李毅%张雪霞%贾英斌%李文华%张百萌
李毅%張雪霞%賈英斌%李文華%張百萌
리의%장설하%가영빈%리문화%장백맹
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
梗阻性黃疸%缺血後處理%缺血再灌註損傷%腎髒%腫瘤壞死因子-α%大鼠
경조성황달%결혈후처리%결혈재관주손상%신장%종류배사인자-α%대서
ischemic postconditioning%ischemia reperfusion injury%kidney%obstructive jaundice%tumor necrosis fac-tor-α%rats
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。
目的:探討缺血後處理對梗阻性黃疸腎缺血再灌註損傷大鼠血清TNF-α水平的影響。方法60隻SD大鼠隨機分成梗阻性黃疸對照組(S組)、梗阻性黃疸腎缺血再灌註組(I/R組)、梗阻性黃疸腎缺血再灌註缺血後處理組(IPO組),每組20隻。根據缺血後再灌註時間點各組又分為再灌註0 h(T0)、1 h(T1)、3 h(T2)、6 h(T3)4箇亞組各5例。檢測再灌註後的各時點血清中尿素氮(BUN)、肌酐(Cr)、TNF-α水平,觀察腎組織的病理改變。結果 I/R組和IPO組血清BUN、Cr、TNF-α水平均高于S組(P均<0.05), IPO組T2時間點血清Cr、BUN、TNF-α水平均低于I/R組( P均<0.05)。結論缺血後處理可以下調大鼠血清TNF-α水平,從而減輕梗阻性黃疸大鼠腎缺血再灌註損傷,其機製可能與抑製炎癥反應有關。
목적:탐토결혈후처리대경조성황달신결혈재관주손상대서혈청TNF-α수평적영향。방법60지SD대서수궤분성경조성황달대조조(S조)、경조성황달신결혈재관주조(I/R조)、경조성황달신결혈재관주결혈후처리조(IPO조),매조20지。근거결혈후재관주시간점각조우분위재관주0 h(T0)、1 h(T1)、3 h(T2)、6 h(T3)4개아조각5례。검측재관주후적각시점혈청중뇨소담(BUN)、기항(Cr)、TNF-α수평,관찰신조직적병리개변。결과 I/R조화IPO조혈청BUN、Cr、TNF-α수평균고우S조(P균<0.05), IPO조T2시간점혈청Cr、BUN、TNF-α수평균저우I/R조( P균<0.05)。결론결혈후처리가이하조대서혈청TNF-α수평,종이감경경조성황달대서신결혈재관주손상,기궤제가능여억제염증반응유관。
Objective To investigate effect of ischemic postconditioning on kidney ischemia-reperfusion injury and the expression of TNF-αin 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), ob-structive 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-αwere collected and ob-served, kidney pathological changes were observed .Results Compared with group S, the serum levels of BUN and Cr in-creased, TNF-αin 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-αdecreased (all P<0.05).Conclusions Ischemic postconditioning can downreg-ulate the expression of TNF-αand alleviate the renal ischemia-reperfusion injury in obstructive jaundice rats , whith may be through inhibiting inflammatory reactions .