中国中西医结合肾病杂志
中國中西醫結閤腎病雜誌
중국중서의결합신병잡지
Chinese Journal of Integrated Traditional and Western Nephrology
2015年
10期
870-873
,共4页
张慧峰%高晓琴%黄轶嵘%于为民%刘静%李荣山
張慧峰%高曉琴%黃軼嶸%于為民%劉靜%李榮山
장혜봉%고효금%황질영%우위민%류정%리영산
肾脏%缺血预处理%缺血再灌注损伤%P38MAPK%iNOS%COX2
腎髒%缺血預處理%缺血再灌註損傷%P38MAPK%iNOS%COX2
신장%결혈예처리%결혈재관주손상%P38MAPK%iNOS%COX2
Kidney%Ischemic preconditioning%Ischemia reperfusion%P38 MAPK%iNOS%COX2
目的:探讨大鼠肾脏缺血预处理中 P38 MAPK、iNOS与 COX2 间的信号转导关系. 方法:雄性 wistar 大鼠66只,随机分为6组,分别为:假手术( sham)组,缺血再灌注( IR)组,缺血预处理+缺血再灌注( IPC)组,SB203580药物干预(SB203580)组,AG药物干预(AG)组,NS398药物干预(NS398)组,在再灌注后24 h、48 h两个时间点取材,用苦味酸法测定血清肌酐反映肾功能变化情况;用Western blot法检测再灌注后48 h肾组织P38 MAPK、iNOS与COX2 蛋白的表达,进行半定量分析. 结果:血肌酐在IPC组较IR组低(P<0. 05)尤其在IPC后48 h明显(P<0. 01);P38MAPK、iNOS与COX2 在sham组,IR组,IPC组均有表达,尤在IPC组表达明显(P<0. 01);在SB203580组无P38MAPK蛋白的表达,iNOS、COX2 的表达均较IPC组低(P<0. 05);在AG组无iNOS蛋白的表达,COX2 蛋白的表达较IPC组低(P<0. 05);在NS398组无COX2 蛋白表达, P38MAPK、iNOS蛋白的表达与IPC组相差不明显(P>0. 05),在 AG与 NS398 组 P38 MAPK蛋白表达与 IPC组相差不明显(P>0.05). 结论:缺血预处理时P38MAPK、iNOS与COX2 蛋白均表达、活化,在其信号转导关系中,P38MAPK是iNOS的上游、并通过iNOS活化介导COX2 表达.
目的:探討大鼠腎髒缺血預處理中 P38 MAPK、iNOS與 COX2 間的信號轉導關繫. 方法:雄性 wistar 大鼠66隻,隨機分為6組,分彆為:假手術( sham)組,缺血再灌註( IR)組,缺血預處理+缺血再灌註( IPC)組,SB203580藥物榦預(SB203580)組,AG藥物榦預(AG)組,NS398藥物榦預(NS398)組,在再灌註後24 h、48 h兩箇時間點取材,用苦味痠法測定血清肌酐反映腎功能變化情況;用Western blot法檢測再灌註後48 h腎組織P38 MAPK、iNOS與COX2 蛋白的錶達,進行半定量分析. 結果:血肌酐在IPC組較IR組低(P<0. 05)尤其在IPC後48 h明顯(P<0. 01);P38MAPK、iNOS與COX2 在sham組,IR組,IPC組均有錶達,尤在IPC組錶達明顯(P<0. 01);在SB203580組無P38MAPK蛋白的錶達,iNOS、COX2 的錶達均較IPC組低(P<0. 05);在AG組無iNOS蛋白的錶達,COX2 蛋白的錶達較IPC組低(P<0. 05);在NS398組無COX2 蛋白錶達, P38MAPK、iNOS蛋白的錶達與IPC組相差不明顯(P>0. 05),在 AG與 NS398 組 P38 MAPK蛋白錶達與 IPC組相差不明顯(P>0.05). 結論:缺血預處理時P38MAPK、iNOS與COX2 蛋白均錶達、活化,在其信號轉導關繫中,P38MAPK是iNOS的上遊、併通過iNOS活化介導COX2 錶達.
목적:탐토대서신장결혈예처리중 P38 MAPK、iNOS여 COX2 간적신호전도관계. 방법:웅성 wistar 대서66지,수궤분위6조,분별위:가수술( sham)조,결혈재관주( IR)조,결혈예처리+결혈재관주( IPC)조,SB203580약물간예(SB203580)조,AG약물간예(AG)조,NS398약물간예(NS398)조,재재관주후24 h、48 h량개시간점취재,용고미산법측정혈청기항반영신공능변화정황;용Western blot법검측재관주후48 h신조직P38 MAPK、iNOS여COX2 단백적표체,진행반정량분석. 결과:혈기항재IPC조교IR조저(P<0. 05)우기재IPC후48 h명현(P<0. 01);P38MAPK、iNOS여COX2 재sham조,IR조,IPC조균유표체,우재IPC조표체명현(P<0. 01);재SB203580조무P38MAPK단백적표체,iNOS、COX2 적표체균교IPC조저(P<0. 05);재AG조무iNOS단백적표체,COX2 단백적표체교IPC조저(P<0. 05);재NS398조무COX2 단백표체, P38MAPK、iNOS단백적표체여IPC조상차불명현(P>0. 05),재 AG여 NS398 조 P38 MAPK단백표체여 IPC조상차불명현(P>0.05). 결론:결혈예처리시P38MAPK、iNOS여COX2 단백균표체、활화,재기신호전도관계중,P38MAPK시iNOS적상유、병통과iNOS활화개도COX2 표체.
Objective:Explore the relations among P38 mitogen-activated protein kinase( P38 MAPK) , nitric synthase ( iN-OS)and cyclooxygenase-2(COX2) in rat renal ischemic preconditioning (IPC). Methods:66 male Wistar rats were randomly divid-ed into 6 groups:sham group ( n=6 ) , ischemic reperfusion ( IR, n=12 ) group, ischemic preconditioning+ischemic reperfusion (IPC,n=12) group, SB203580 (inhibitor of P38MAPK) group(n=12), AG(inhibitor of iNOS) group (n=12), NS398 (inhibitor of COX2) group (n=12). Rats were sacrificed, serum and kidney were collected at 24 and 48 h after reperfusion. The renal function was evaluated by testing serum creatinine level. The expression of P38 MAPK, iNOS and COX2 in the kidney was determined by West-ern blotting. Results:The animals in IPC group showed lower serum creatinine compared with IR group (P<0. 05). The difference was more significant in IPC group at 48 h (P<0. 01). P38MAPK, iNOS and COX2 were expressed in all groups, in which IPC group showed the highest expression level. There was no P38 MAPK in SB203580 group, and the expression of iNOS and COX2 are lower. (P<0. 05) compared with IPC group;No iNOS expressed in AG group, and the expression of COX2 was significantly less than IPC group (P<0. 05); There are no COX2 expression in NS398 group, P38 MAPK and iNOS were not significantly different from IPC group. (P>0. 05); As far as as P38 MAPK expression was concerned, there was no significant deference in AG、NS398 and IPC group (P>0. 05). Conclusion:Ischemic preconditioning showed protective effect in 48 hours post-ischemia reperfusion. The pro-tection was related to P38 MAPK, iNOS and COX2 expression、activation. P38 MAPK is the upstream of iNOS, and upregulated COX2 expression by activating iNOS.