中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2013年
6期
722-724
,共3页
姚星%王焱林%何祥虎%张宗泽%颜学滔
姚星%王焱林%何祥虎%張宗澤%顏學滔
요성%왕염림%하상호%장종택%안학도
血红素氧化酶(脱环)%再灌注损伤%肾%细胞穿透肽
血紅素氧化酶(脫環)%再灌註損傷%腎%細胞穿透肽
혈홍소양화매(탈배)%재관주손상%신%세포천투태
Heme oxygenase (decyclizing)%Reperfusion injury%Kidney%Cell penetrating peptide
目的 评价细胞穿透肽PEP-1导入血红素加氧酶-1(HO-1)蛋白对大鼠肾缺血再灌注损伤的影响.方法 健康雄性SD大鼠18只,周龄7～9周,体重210 ～ 260 g,采用随机数字表法,将其随机分为3组(n=6):假手术组(S组)、肾缺血再灌注组(I/R组)和融合蛋白PEP-1/HO-1+肾缺血再灌注组(HO组).采用夹闭双侧肾动脉45 min恢复灌注的方法制备大鼠肾缺血再灌注损伤模型.HO组于夹闭双侧肾动脉前30 min时静脉注射融合蛋白PEP-1/HO-1.于再灌注6h时取右侧颈总动脉血样,测定血清BUN和Cr浓度；取肾组织检测MDA含量和SOD活性；采用免疫组化法检测肾组织HO-1的表达.结果 与S组比较,I/R组和HO组肾组织MDA含量、血清BUN和Cr浓度升高,肾组织SOD活性降低,HO-1蛋白表达上调(P＜0.05)；与I/R组比较,HO组肾组织MDA含量、血清BUN和Cr浓度降低,肾组织SOD活性升高,HO-1蛋白表达上调(P＜0.05).结论 细胞穿透肽PEP-1将HO-1蛋白成功导入肾组织,导入的HO-1蛋白通过抑制脂质过氧化反应减轻肾缺血再灌注损伤.
目的 評價細胞穿透肽PEP-1導入血紅素加氧酶-1(HO-1)蛋白對大鼠腎缺血再灌註損傷的影響.方法 健康雄性SD大鼠18隻,週齡7～9週,體重210 ～ 260 g,採用隨機數字錶法,將其隨機分為3組(n=6):假手術組(S組)、腎缺血再灌註組(I/R組)和融閤蛋白PEP-1/HO-1+腎缺血再灌註組(HO組).採用夾閉雙側腎動脈45 min恢複灌註的方法製備大鼠腎缺血再灌註損傷模型.HO組于夾閉雙側腎動脈前30 min時靜脈註射融閤蛋白PEP-1/HO-1.于再灌註6h時取右側頸總動脈血樣,測定血清BUN和Cr濃度；取腎組織檢測MDA含量和SOD活性；採用免疫組化法檢測腎組織HO-1的錶達.結果 與S組比較,I/R組和HO組腎組織MDA含量、血清BUN和Cr濃度升高,腎組織SOD活性降低,HO-1蛋白錶達上調(P＜0.05)；與I/R組比較,HO組腎組織MDA含量、血清BUN和Cr濃度降低,腎組織SOD活性升高,HO-1蛋白錶達上調(P＜0.05).結論 細胞穿透肽PEP-1將HO-1蛋白成功導入腎組織,導入的HO-1蛋白通過抑製脂質過氧化反應減輕腎缺血再灌註損傷.
목적 평개세포천투태PEP-1도입혈홍소가양매-1(HO-1)단백대대서신결혈재관주손상적영향.방법 건강웅성SD대서18지,주령7～9주,체중210 ～ 260 g,채용수궤수자표법,장기수궤분위3조(n=6):가수술조(S조)、신결혈재관주조(I/R조)화융합단백PEP-1/HO-1+신결혈재관주조(HO조).채용협폐쌍측신동맥45 min회복관주적방법제비대서신결혈재관주손상모형.HO조우협폐쌍측신동맥전30 min시정맥주사융합단백PEP-1/HO-1.우재관주6h시취우측경총동맥혈양,측정혈청BUN화Cr농도；취신조직검측MDA함량화SOD활성；채용면역조화법검측신조직HO-1적표체.결과 여S조비교,I/R조화HO조신조직MDA함량、혈청BUN화Cr농도승고,신조직SOD활성강저,HO-1단백표체상조(P＜0.05)；여I/R조비교,HO조신조직MDA함량、혈청BUN화Cr농도강저,신조직SOD활성승고,HO-1단백표체상조(P＜0.05).결론 세포천투태PEP-1장HO-1단백성공도입신조직,도입적HO-1단백통과억제지질과양화반응감경신결혈재관주손상.
Objective To investigate the effects of heme oxygenase-1 (HO-1) transduced by cell penetrating peptide PEP-1 on renal ischemia/reperfusion (I/R) injury in rats.Methods Eighteen male Sprague-Dawley rats,aged 7-9 weeks,weighing 210-260 g,were randomly divided into 3 groups (n =6 each):sham operation group (group S),renal I/R injury group (group I/R) and fusion protein PEP-1/HO-I + I/R group (group HO).I/R injury was produced by occluding bilateral renal arteries for 45 min followed by reperfusion for 6 h.The fusion protein PEP-1/HO-1 was injected via the left iliac vein 30 min prior to ischemia in group HO.Bilateral renal arteries were only exposed but not occluded in group C.Blood samples were collected from the right common carotid artery at 6 h of reperfusion for determination of serum blood urea nitrogen (BUN) and creatinine (Cr) concentrations.The malondialdehyde (MDA) content,superoxide dismutase (SOD) activity and HO-1 expression in renal tissues were measured.Results Compared with group S,the levels of MDA,serum BUN and Cr were significantly increased,the SOD activity was decreased,and HO-1 expression was up-regulated in groups I/R and HO (P ＜0.05).Compared with group I/R,the levels of MDA,serum BUN and Cr were significantly decreased,the SOD activity was increased,and HO-1 expression was up-regulated in group HO (P ＜ 0.05).Conclusion HO-1 protein can be successfully transduced into renal tissues by PEP-1 and transduced HO-1 protein reduces renal I/R injury by inhibiting lipid peroxidation response.
