中国基层医药
中國基層醫藥
중국기층의약
CHINESE JOURNAL OF PRIMARY MEDICINE AND PHARMACY
2012年
15期
2241-2243
,共3页
李韶南%黄慧芳%李广镰%刘震%陈平安
李韶南%黃慧芳%李廣鐮%劉震%陳平安
리소남%황혜방%리엄렴%류진%진평안
缺血-再灌注损伤%后适应%骨骼肌%凋亡
缺血-再灌註損傷%後適應%骨骼肌%凋亡
결혈-재관주손상%후괄응%골격기%조망
Ischemia reperfusion injury%Postconditioning%Skeletal muscle%Apoptosis
目的 观察缺血后适应(IPC)减轻急性下肢缺血(AU)再灌注损伤的疗效并探讨其机制.方法 将45只新西兰大白兔采用高脂饮食与动脉内膜球囊损伤结合的方式建立下肢动脉粥样硬化狭窄动物模型,随机分为对照组、缺血再灌注组(IR组)、缺血后适应组(IPC组),每组各15只.检测三组大白兔阻断股动脉前、持续再灌注2h后血液中肌酸激酶(CK)、丙二醛(MDA)、超氧化物岐化酶(SOD)水平,观察再灌注后下肢骨骼肌组织学改变,并采用原位末端标记法(TUNEL)分析三组大白兔下肢再灌注后骨骼肌细胞凋亡情况.结果 与IR组比较,IPC组兔血浆CK、MDA明显降低[(7.49±0.84) U/L与(8.19±1.06) U/L,P<0.05],[(3.67±0.36) nmol/L与(4.06±0.55) nmol/L,P<0.05],而SOD则显著升高[(420.40±30.94)μmol/L与(384.73±44.12) μmol/L,P<0.05],骨骼肌细胞凋亡指数降低[(12.27±2.11)%与(16.62±1.44)%,P<0.01],差异有统计学意义,并且组织形态学观察IPC组兔骨骼肌损伤、坏死程度较IR组减轻.结论 急性下肢缺血应用IPC能显著减轻下肢缺血再灌注损伤,其机制与减少自由基生成、增强抗氧化及减轻缺血再灌注诱导的骨骼肌细胞凋亡有关.
目的 觀察缺血後適應(IPC)減輕急性下肢缺血(AU)再灌註損傷的療效併探討其機製.方法 將45隻新西蘭大白兔採用高脂飲食與動脈內膜毬囊損傷結閤的方式建立下肢動脈粥樣硬化狹窄動物模型,隨機分為對照組、缺血再灌註組(IR組)、缺血後適應組(IPC組),每組各15隻.檢測三組大白兔阻斷股動脈前、持續再灌註2h後血液中肌痠激酶(CK)、丙二醛(MDA)、超氧化物岐化酶(SOD)水平,觀察再灌註後下肢骨骼肌組織學改變,併採用原位末耑標記法(TUNEL)分析三組大白兔下肢再灌註後骨骼肌細胞凋亡情況.結果 與IR組比較,IPC組兔血漿CK、MDA明顯降低[(7.49±0.84) U/L與(8.19±1.06) U/L,P<0.05],[(3.67±0.36) nmol/L與(4.06±0.55) nmol/L,P<0.05],而SOD則顯著升高[(420.40±30.94)μmol/L與(384.73±44.12) μmol/L,P<0.05],骨骼肌細胞凋亡指數降低[(12.27±2.11)%與(16.62±1.44)%,P<0.01],差異有統計學意義,併且組織形態學觀察IPC組兔骨骼肌損傷、壞死程度較IR組減輕.結論 急性下肢缺血應用IPC能顯著減輕下肢缺血再灌註損傷,其機製與減少自由基生成、增彊抗氧化及減輕缺血再灌註誘導的骨骼肌細胞凋亡有關.
목적 관찰결혈후괄응(IPC)감경급성하지결혈(AU)재관주손상적료효병탐토기궤제.방법 장45지신서란대백토채용고지음식여동맥내막구낭손상결합적방식건립하지동맥죽양경화협착동물모형,수궤분위대조조、결혈재관주조(IR조)、결혈후괄응조(IPC조),매조각15지.검측삼조대백토조단고동맥전、지속재관주2h후혈액중기산격매(CK)、병이철(MDA)、초양화물기화매(SOD)수평,관찰재관주후하지골격기조직학개변,병채용원위말단표기법(TUNEL)분석삼조대백토하지재관주후골격기세포조망정황.결과 여IR조비교,IPC조토혈장CK、MDA명현강저[(7.49±0.84) U/L여(8.19±1.06) U/L,P<0.05],[(3.67±0.36) nmol/L여(4.06±0.55) nmol/L,P<0.05],이SOD칙현저승고[(420.40±30.94)μmol/L여(384.73±44.12) μmol/L,P<0.05],골격기세포조망지수강저[(12.27±2.11)%여(16.62±1.44)%,P<0.01],차이유통계학의의,병차조직형태학관찰IPC조토골격기손상、배사정도교IR조감경.결론 급성하지결혈응용IPC능현저감경하지결혈재관주손상,기궤제여감소자유기생성、증강항양화급감경결혈재관주유도적골격기세포조망유관.
Objective To study the effects of ischemia postconditioning(IPC) in reducing ischemia-reperfusion injury(IRI) in acute limp ischemia(ALI) and investigate the mechanism.Methods 45 New Zealand rabbits were treated with the method that combined high lipid diets and femoral intima injury by balloon inflation to build up limp atherosclerotic stenosis model,then they were randomly divided into three groups( each group 15 rabbits):control group;IR group and IPC group.Serum creatine phosphate kinase(CK),malondialehyde(MDA),superoxide dismutase (SOD) in three groups were measured before occlusion and 2 hours after sustaining reperfusion.The histological changes of limp skeletal muscle of experimental rabbits were analyzed and TUNEL method was used to access apoptosis of skeletal muscle cells.Results The levels of CK,M DA in IPC group were lower than IR group [ (7.49 ± 0.84)vs (8.19 ± 1.06),P<0.05],[ (3.67 ±0.36) vs (4.06 ±0.55),P <0.05] while SOD level was higher than IR group [ (420.40 ± 30.94 ) vs ( 384.73 ± 44.12),P < 0.05 ] ; The injury of skeletal muscles in I PC group was lighter than IR group and the apoptosis index of skeletal muscle cells was significantly decreased compared with that in IR group[(12.27+2.11)% vs (16.62 ± 1.44)%,P<0.01].Conclusion Applying IPC in acute limp ischemia could alleviate IRI and protect skeletal muscles.The mechanism was associated with oxidation resistance enhancing and the effects in reducing apoptosis of skeletal muscles induced by IRI.