中国医药
中國醫藥
중국의약
CHINA MEDICINE
2012年
6期
689-692
,共4页
邢莉%潘旭东%吕英谦%赵莉%李虎臣
邢莉%潘旭東%呂英謙%趙莉%李虎臣
형리%반욱동%려영겸%조리%리호신
缺血再灌注%肠损伤%远端缺血预适应%聚腺苷二磷酸核糖聚合酶-1
缺血再灌註%腸損傷%遠耑缺血預適應%聚腺苷二燐痠覈糖聚閤酶-1
결혈재관주%장손상%원단결혈예괄응%취선감이린산핵당취합매-1
Ischemia-reperfusion%Intestinal injure%Remote ischemic preconditioning%Poly ( ADP-ribose) polymerase-1
目的 通过建立大鼠远端缺血预适应(RIPC)和肠缺血再灌注损伤模型,探讨RIPC对肠缺血再灌注损伤是否有防护作用.方法 雄性SD大鼠分为肠缺血再灌注(L/R)组(8只)、RIPC组(8只)和假手术组(Sham组,5只).用充气套囊加压阻断右侧上下肢体血供5 min后放气恢复血供5 min的方法重复3次首先建立大鼠肢体缺血预适应模型.后经正中剖腹,阻断腹腔干动脉和肠系膜上动脉30 min后,恢复血运2h制作鼠肠缺血再灌注模型.取肠组织分别作苏木素-伊红染色、聚腺苷二磷酸核糖(PAR)免疫组织化学染色、原位凋亡检测、髓过氧化酶( MPO)活性和丙二醛检测.结果 肠组织损伤评分、PAR阳性表达率、MPO活性和丙二醛水平,I/R组均较Sham组明显增高[(4.65±0.82)分比(0.56±0.48)分,(23.8±2.8)％比(5.1±0.8)％；(330±15)U/g比(24±5)U/g；(248±15)μmol/( L· mg)比(36±7)μmol/(L·mg),均P＜0.05]；RIPC组上述指标[(2.92±0.74),(16.8±3.1)％,(218±17) U/g,(121±13) μmol/(L· mg)]均明显低于I/R组,但仍高于Sham组(P＜0.05).结论 RIPC可能会通过抑制肠炎症反应、脂质过氧化和降低PARP激活程度来减轻I/R后小肠组织损伤.
目的 通過建立大鼠遠耑缺血預適應(RIPC)和腸缺血再灌註損傷模型,探討RIPC對腸缺血再灌註損傷是否有防護作用.方法 雄性SD大鼠分為腸缺血再灌註(L/R)組(8隻)、RIPC組(8隻)和假手術組(Sham組,5隻).用充氣套囊加壓阻斷右側上下肢體血供5 min後放氣恢複血供5 min的方法重複3次首先建立大鼠肢體缺血預適應模型.後經正中剖腹,阻斷腹腔榦動脈和腸繫膜上動脈30 min後,恢複血運2h製作鼠腸缺血再灌註模型.取腸組織分彆作囌木素-伊紅染色、聚腺苷二燐痠覈糖(PAR)免疫組織化學染色、原位凋亡檢測、髓過氧化酶( MPO)活性和丙二醛檢測.結果 腸組織損傷評分、PAR暘性錶達率、MPO活性和丙二醛水平,I/R組均較Sham組明顯增高[(4.65±0.82)分比(0.56±0.48)分,(23.8±2.8)％比(5.1±0.8)％；(330±15)U/g比(24±5)U/g；(248±15)μmol/( L· mg)比(36±7)μmol/(L·mg),均P＜0.05]；RIPC組上述指標[(2.92±0.74),(16.8±3.1)％,(218±17) U/g,(121±13) μmol/(L· mg)]均明顯低于I/R組,但仍高于Sham組(P＜0.05).結論 RIPC可能會通過抑製腸炎癥反應、脂質過氧化和降低PARP激活程度來減輕I/R後小腸組織損傷.
목적 통과건립대서원단결혈예괄응(RIPC)화장결혈재관주손상모형,탐토RIPC대장결혈재관주손상시부유방호작용.방법 웅성SD대서분위장결혈재관주(L/R)조(8지)、RIPC조(8지)화가수술조(Sham조,5지).용충기투낭가압조단우측상하지체혈공5 min후방기회복혈공5 min적방법중복3차수선건립대서지체결혈예괄응모형.후경정중부복,조단복강간동맥화장계막상동맥30 min후,회복혈운2h제작서장결혈재관주모형.취장조직분별작소목소-이홍염색、취선감이린산핵당(PAR)면역조직화학염색、원위조망검측、수과양화매( MPO)활성화병이철검측.결과 장조직손상평분、PAR양성표체솔、MPO활성화병이철수평,I/R조균교Sham조명현증고[(4.65±0.82)분비(0.56±0.48)분,(23.8±2.8)％비(5.1±0.8)％；(330±15)U/g비(24±5)U/g；(248±15)μmol/( L· mg)비(36±7)μmol/(L·mg),균P＜0.05]；RIPC조상술지표[(2.92±0.74),(16.8±3.1)％,(218±17) U/g,(121±13) μmol/(L· mg)]균명현저우I/R조,단잉고우Sham조(P＜0.05).결론 RIPC가능회통과억제장염증반응、지질과양화화강저PARP격활정도래감경I/R후소장조직손상.
Objective To investigate the effect of remote ischemic preconditioning (RICP) on intestinal is-chemia-reperfusion (I/R) injury in a rat model.Methods The model of remote ischemic preconditioning in rats was made by 3 × 5-min cycles of right upper arm/leg ischemia and 5-min reperfusion.Then intestinal I/R was established by clamping both the celiac trunk and the superior mesenteric artery for 30 min,foflowed by reperfusion for 2h.The animals were assigned to different groups:I/R group,RICP group and Sham group.The morphological changes of intestine,PARP-1 activation,apoptosis were detected by means of HE,immunohistochemical staining for poly (ADP-ribose) and TUNEL.Regional inflammatory reaction and lipid peroxidation were indicated by myeloperoxidase (MPO) activity and malonaldehyde (MDA).Results In I/R group,the extent of intestinal injure and PARP-1 activation,Compared with Sham group,TUNEL positive-staining,MPO activity and MDA were elevated significantly in I/R group [ (4.65 ± 0.82) vs (0.56 ± 0.48 ),( 23.8 ± 2.8 ) ％ vs ( 5.1 ± 0.8 ) ％ ; ( 330 ± 15 ) U/g vs (24 ±5)U/g;(248 ±15)μnol/(L · mg) vs (36 ±7)μmol/(L · mg),P＜0.05) ].In RICP group,these variables [ (2.92 ±0.74),( 16.8 ±3.1)％,(218 ± 17)U/g,(121 ± 13) μmol/(L · mg) ] were statistically lower than those in I/R group( P ＜ 0.05 ),but higher than those of Sham group ( P ＜ 0.05 ).Conclusion These findings demonstrat that RICP has the potential protection from intestinal I/R,which could be induced by inhibiting regional inflammatory reaction,lipid peroxidation and PARP-1 activation.
