中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2013年
5期
606-608
,共3页
何祥虎%颜学滔%王焱林%王成夭%张宗泽
何祥虎%顏學滔%王焱林%王成夭%張宗澤
하상호%안학도%왕염림%왕성요%장종택
血红素加氧酶-1%细胞穿透肽%再灌注损伤%小肠%肝
血紅素加氧酶-1%細胞穿透肽%再灌註損傷%小腸%肝
혈홍소가양매-1%세포천투태%재관주손상%소장%간
Heme Oxygenase-1%Cell penetrating peptide%Reperfusion injury%Intestine,small%Liver
目的 评价细胞穿透肽PEP-1介导的血红素加氧酶-1(HO-1)对大鼠肠缺血再灌注诱发肝损伤的影响.方法 雄性SD大鼠24只,7~9周龄,体重210~260 g,采用随机数字表法,将其分为3组(n=8):假手术组(S组)、肠缺血再灌注组(I/R组)和融合蛋白PEP-1/HO-1组(HO组).采用夹闭肠系膜上动脉45 min,恢复灌注120 min的方法制备大鼠肠缺血再灌注模型.HO组于缺血前30 min经左侧髂静脉注射融合蛋白PEP-1/HO-1 0.5 mg,S组仅分离闭肠系膜上动脉,但不夹闭.于再灌注120 min时,右侧颈总动脉取血样,测定血清AST和ALT的活性;然后处死大鼠,取肝组织,光镜下观察病理学结果,测定MDA含量和SOD活性.结果 与S组比较,I/R组和HO组血清AST和ALT的活性升高,肝组织MDA含量升高,SOD活性降低(P<0.05);与I/R组比较,HO组血清AST和ALT的活性降低,肝组织MDA含量降低,SOD活性升高(P<0.05),肝损伤减轻.结论 细胞穿透肽PEP-1介导的HO-1可减轻大鼠肠缺血再灌注诱发的肝损伤.
目的 評價細胞穿透肽PEP-1介導的血紅素加氧酶-1(HO-1)對大鼠腸缺血再灌註誘髮肝損傷的影響.方法 雄性SD大鼠24隻,7~9週齡,體重210~260 g,採用隨機數字錶法,將其分為3組(n=8):假手術組(S組)、腸缺血再灌註組(I/R組)和融閤蛋白PEP-1/HO-1組(HO組).採用夾閉腸繫膜上動脈45 min,恢複灌註120 min的方法製備大鼠腸缺血再灌註模型.HO組于缺血前30 min經左側髂靜脈註射融閤蛋白PEP-1/HO-1 0.5 mg,S組僅分離閉腸繫膜上動脈,但不夾閉.于再灌註120 min時,右側頸總動脈取血樣,測定血清AST和ALT的活性;然後處死大鼠,取肝組織,光鏡下觀察病理學結果,測定MDA含量和SOD活性.結果 與S組比較,I/R組和HO組血清AST和ALT的活性升高,肝組織MDA含量升高,SOD活性降低(P<0.05);與I/R組比較,HO組血清AST和ALT的活性降低,肝組織MDA含量降低,SOD活性升高(P<0.05),肝損傷減輕.結論 細胞穿透肽PEP-1介導的HO-1可減輕大鼠腸缺血再灌註誘髮的肝損傷.
목적 평개세포천투태PEP-1개도적혈홍소가양매-1(HO-1)대대서장결혈재관주유발간손상적영향.방법 웅성SD대서24지,7~9주령,체중210~260 g,채용수궤수자표법,장기분위3조(n=8):가수술조(S조)、장결혈재관주조(I/R조)화융합단백PEP-1/HO-1조(HO조).채용협폐장계막상동맥45 min,회복관주120 min적방법제비대서장결혈재관주모형.HO조우결혈전30 min경좌측가정맥주사융합단백PEP-1/HO-1 0.5 mg,S조부분리폐장계막상동맥,단불협폐.우재관주120 min시,우측경총동맥취혈양,측정혈청AST화ALT적활성;연후처사대서,취간조직,광경하관찰병이학결과,측정MDA함량화SOD활성.결과 여S조비교,I/R조화HO조혈청AST화ALT적활성승고,간조직MDA함량승고,SOD활성강저(P<0.05);여I/R조비교,HO조혈청AST화ALT적활성강저,간조직MDA함량강저,SOD활성승고(P<0.05),간손상감경.결론 세포천투태PEP-1개도적HO-1가감경대서장결혈재관주유발적간손상.
Objective To evaluate the effects of heme oxygenase-1 (HO-1) mediated by cell penetrating peptide PEP-1 on liverinjury induced by intestinal ischemia/reperfusion (I/R) in rats.Methods Twenty-four male Sprague-Dawley rats,aged 7-9 weeks,weighing 210-260 g,were randomly divided into 3 groups (n =8 each):sham operation group (group S),intestinal I/R group (group I/R) and PEP-1/HO-1 group (group HO).To establish a model of intestinal I/R,intestines were exteriorized and the superior mesenteric artery was exposed and occluded for 45 min ischemia,and then the clamp was removed for 120 min reperfusion.The PEP-1/HO-1 fusion protein 0.5 mg was injectedvia ihe left iliac vein 30 min prior to ischemia in group HO.The superior mesenteric artery was only exposed but not occluded in group S.At the end of reperfusion,blood samples were collected from the right common carotid artery for measurement of serum aspartate aminotransferase (AST),alanine aminotransferase (ALT) activities.The rats were then sacrificed and livers were removed for microscopic examination and for determination of malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in livertissues.Results Compared with group S,serum AST and ALT activities and MDA content in liver tissues were significantly increased,while SOD activity in liver tissues was decreased in groups I/R and HO (P < 0.05).Compared with group I/R,serum AST and ALT activities and MDA content in liver tissues were significantly decreased,while SOD activity in liver tissues was increased in group HO (P <0.05).Liver injury induced by intestinal I/R was significantly attenuated in group HO compared with group I/R (P < 0.05).Conciusioon HO-1 protein mediated by cell penetrating peptide PEP-1 can attenuate liver injury induced by intestinalI/R in rats.