预适应联合后适应对大鼠缺血再灌注损伤的保护作用

Protective Effects of Preconditioning Combined with Post Adaptation on Cerebral Ischemia and Reperfusion Injury in Rats

目的探讨预适应联合后适应对大鼠脑缺血再灌注损伤的保护作用。方法该实验于2015年10月—2016年9月进行。选取清洁级雄性SD大鼠50只,体重(270±30)g(内蒙古科技大学包头医学院动物中心提供,合格证号:201407413,dd Y系SPF级);随机分为假手术组、模型组、预适应组、后适应组和预适应+后适应组,每组10只,除假手术组外,其余各组大鼠均制作为脑缺血/再灌注损伤模型,在再灌注48 h后,检测各组大鼠神经功能、脑梗死灶体检、脑组织氧化应激损伤生化指标及神经元凋亡情况。结果再灌注12、24 h和48 h模型组神经功能缺陷评分(3.10±0.23)分、(3.53±0.15)分、(3.32±0.16)分明显高于其他处理组(P<0.05);再灌注12、24 h和48 h处理组中,预适应+后适应组神经功能缺陷评分最低(1.89±0.11)分、(1.75±0.12)分、(1.22±0.13)分(P<0.05);预适应+后适应组脑梗死灶体积为(100.41±33.26)mm3,明显低于模型组、预适应组和后适应组(P<0.05);预适应组(182.43±50.10)mm3和后适应组(185.10±52.33)mm3脑梗死灶体积较模型组(100.41±33.26)mm3降低(P<0.05);假手术组超氧化物歧化酶(SOD)活性(122.41±24.61)μn/mgprot明显高于模型组(45.56±10.31)μn/mgprot,而丙二醛(MDA)(43.51±9.64)nmol/mgprot低于模型组(113.43±21.07)nmol/mgprot(P<0.05);后适应组(76.81±9.83)μn/mgprot和预适应后适应组SOD活性较模型组升高(110.13±12.16)μn/mgprot,而MDA(61.51±12.15)nmol/mgprot较模型组(113.43±21.07)nmol/mgprot降低(P<0.05);假手术组细胞凋亡数(15.20±7.62)个明显低于模型组(84.11±8.42)个(P<0.05);各处理组细胞凋亡数较模型组有所降低(73.04±9.01)个、(61.12±10.17)个(P<0.05),其中预适应+后适应组神经元细胞凋亡数最少,为(47.20±9.21)个。结论预适应和后适应均能对大鼠脑缺血再灌注损伤具有保护作用,而两者联合应用能进一步加强保护作用。

the rats were random ly divided into sham operation group,model group,pre-ad ap tatio n group,post adaptation group and preconditioning+post adaptation group,with 10 rats in each group,except sham operation group,other groups were m ade into cerebral ischem ia/reperfusion injury model,after 48h of reperfusion,each groups rat neurological function was detected,cerebral infarction,brain tissueObjective This paper tries to investigate protective effects of preconditioning com bined with post adaptation on cerebral ischem ia and reperfusion injury in rats.Methods The experim ent was im plem ented from O ctober 2015 to Septem ber 2016.50 clean grade m ale SD rats were selected weight for(270±30)g(provided by Inner M ongolia U niversity of Science and Technology,Baotou M edical College A nim al Center,certificate num ber:201407413,ddY departm ent,SPF grade),oxidative stress injury biochem ical indicators and neuronal apoptosis in rats were observed.Results R eperfusion for 12,24 h and 48 h,the model group of nerve function defect score w as(3.1 0±0.2 3)p o in ts,(3.5 3±0.1 5)p o in ts,(3.3 2±0.1 6)p o in ts,significantly higher than that of other groups(P<0.05);Reperfusion for 12,24 h and 48 h,preconditioning+post adaptation group neural function defect score was(1.89±0.11)points,(1.75±0.12)points,(1.22±0.13)points,(P<0.05);the preconditioning group+postconditioning group was(100.41±33.26)m m 3,which was significantly lower than that in the model group,and the preconditioning group and the postconditioning group(P<0.05).The pretreatm ent group was(182.43±50.10)m m 3 and the postconditioning group was(185.10±52.33)m m 3 and the model group was(100.41±33.26)m m 3(P<0.05).The activity of superoxide dism utase(SOD)was(122.41±24.61)滋n/m gprot in sham operation group,significantly higher than that in model group of(45.56±10.31)滋n/m gprot,while that of m alondialdehyde(MDA)was(43.51±9.64)nm ol/m gprot,significantly lower than that in model group of(113.43±21.07)nm ol/m gprot(P<0.05),the post adaptation group was(76.81±9.83)nm ol/m gprot,and the preconditional group土The activity of SOD in the postconditioning group w as(110.13±12.16)滋n/m gprot,MDA w as(61.51土12.15)nm ol/m gprot,lower than the model group of(113.43±21.07)nm ol/m gprot,(P<0.05);The num ber of apoptotic cells in sham operation group was(15.20±7.62),significantly lower than that in model group of(84.11±8.42)(P<0.05).The num ber of apoptotic cells in each treatm ent group was significantly lower than that in m odel group of(73.04±9.01),(61.12±10.17)(P<0.05),and the num ber of neurons in the pretreatm ent group was the lowest of(47.20±9.21).Conclusion Preconditioning and post adaptation can protect the cerebral ischem ia/reperfusion injury in rats,and the com bined application of the two m ethods can further strengthen the protective effect.