控制性低压后处理对兔脊髓缺血再灌注损伤的影响及其机制探讨

摘要

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.%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。