CAJ | 학술논문

目的：探讨控制性低压后处理对兔脊髓缺血再灌注损伤的影响及机制。方法32只雄性日本大耳白兔随机分为4组，每组8只，分别为假手术对照组（S组）、缺血再灌注损伤组（I/R组）、控制性低压后处理组（P组）、控制性低压后处理＋ERK1/2抑制剂PD98059组（ PD组）。于再灌注后24 h处死动物，取L3～5段脊髓组织标本。TUNEL法检测细胞凋亡；免疫细胞化学SP法检测脊髓组织p-ERK1/2、Caspase-3；羟胺法测定脊髓组织超氧化物歧化酶（SOD），硫代巴比妥酸法测定脊髓组织丙二醛（MDA）。结果与I/R组比较，P组凋亡指数降低，脊髓组织MDA降低、SOD增加、Caspase-3减少、p-ERK1/2增加，P均＜0．05；与P组比较，PD组凋亡指数升高，脊髓组织MDA增加、SOD减少、Caspase-3增加、p-ERK1/2减少，P均＜0．05。结论控制性低压后处理对脊髓缺血再灌注损伤具有保护作用，其机制可能与活化ERK1/2、抑制Caspase-3有关。
목적：탐토공제성저압후처리대토척수결혈재관주손상적영향급궤제。방법32지웅성일본대이백토수궤분위4조，매조8지，분별위가수술대조조（S조）、결혈재관주손상조（I/R조）、공제성저압후처리조（P조）、공제성저압후처리＋ERK1/2억제제PD98059조（ PD조）。우재관주후24 h처사동물，취L3～5단척수조직표본。TUNEL법검측세포조망；면역세포화학SP법검측척수조직p-ERK1/2、Caspase-3；간알법측정척수조직초양화물기화매（SOD），류대파비타산법측정척수조직병이철（MDA）。결과여I/R조비교，P조조망지수강저，척수조직MDA강저、SOD증가、Caspase-3감소、p-ERK1/2증가，P균＜0．05；여P조비교，PD조조망지수승고，척수조직MDA증가、SOD감소、Caspase-3증가、p-ERK1/2감소，P균＜0．05。결론공제성저압후처리대척수결혈재관주손상구유보호작용，기궤제가능여활화ERK1/2、억제Caspase-3유관。
Objective To investigate the effect of controlled low-pressure perfusion postconditioning on the spinal cord ischemia-reperfusion injury in rabbits and the mechanism .Methods Thirty-two Japanese white rabbits were randomly di-vided into four groups (n=8): the sham group (group S), ischemia-reperfusion (I/R) group, controlled low-pressure perfusion postconditioning group (group P), controlled low-pressure perfusion postconditioning +PD98059 (PD) group. All rabbits were sacrificed 24 h after reperfusion , L3-5 segments of the spinal cord were removed .TUNEL method was used to detect the apoptosis , the expression of p-ERK 1/2 and caspase-3 in the spinal cord tissues was detected by immunohisto-chemical SP method , the superoxide dismutase ( SOD) was determined by hydroxylamine method , and the malonyldialde-hyde ( MDA) in the spinal cord tissues was detected by thiobarbituric acid method .Results Compared with I/R group, the apoptosis index decreased, and in the spinal cord tissues, MDA decreased, SOD increased, caspase-3 decreased, p-ERK1/2 increased in the group P (all P<0.05);compared with group P, the apoptosis index increased , and in the spinal cord tissues, MDA increased, SOD decreased, caspase-3 increased, p-ERK1/2 decreased in the PD group ( all P <0.05).Conclusions Controlled low-pressure perfusion postconditioning has the protective effect on the spinal cord I /R injury, whose mechanism may be related to activation of ERK 1/2 pathway and inhibition of the expression of caspase-3.