电针预处理对脑缺血再灌注大鼠HO-1表达及脑血流、神经功能、脑梗死体积的影响

Effects of electroacupuncture pretreatment on the expression of HO-1,cerebral blood flow,neural function and cerebral infarction volume in cerebral ischemia-reperfusion rats

目的观察电针预处理对脑缺血再灌注损伤大鼠血清血红素氧合酶-1(HO-1)表达以及脑血流量、神经功能、脑梗死体积的影响。方法27只成年雄性SD大鼠按照随机数字表法分为假手术组、模型组和电针预处理组,每组各9只。假手术组除不插入线栓外,其余同模型组;模型组造模前束缚14 d,采用线栓法制备大脑中动脉缺血再灌注模型;电针预处理组在造模前14 d行EA预处理,其余同模型组。比较大鼠造模即刻、造模后和再灌注后的脑血流量,造模后24 h的Bederson评分、改良神经功能缺损评分(mNSS)及脑梗死体积;采用Morris水迷宫实验测试空间学习记忆能力;并采用酶联免疫吸附试验检测血清HO-1浓度变化。结果造模即刻,造模后60、120 min,再灌注即刻,再灌注后10、20、30 min,与假手术组比较,模型组大鼠脑血流量明显降低,差异均有统计学意义(P<0.05);与模型组比较,电针预处理组大鼠脑血流量明显升高,差异均有统计学意义(P<0.05)。造模后24 h,与假手术组比较,模型组大鼠Bederson评分、mNSS评分增加,差异均有统计学意义(P<0.05);与模型组比较,电针预处理组Bederson评分、mNSS评分均降低,差异均有统计学意义(P<0.05)。造模后24 h,假手术组TTC染色无梗死灶形成,模型组与电针预处理组均可见不同程度灰白色梗死灶。与模型组比较,电针预处理组脑梗死占比明显减小,差异有统计学意义(P<0.05)。假手术组与模型组大鼠的第四象限滞留时间百分比和血清HO-1水平比较,差异均无统计学意义(P>0.05);与模型组比较,电针预处理组大鼠的第四象限滞留时间百分比和血清HO-1水平均明显升高,差异均有统计学意义(P<0.05)。结论电针预处理可有效恢复脑血流,改善神经缺损功能,减小脑梗死体积,提高认知水平,从而在脑缺血再灌注损伤中发挥一定的保护作用。其机制可能与提高模型大鼠血清中HO-1蛋白表达水平发挥抗氧化应激作用有关。

Objective To observe the effect of electroacupuncture(EA)pretreatment on serum HO-1 expression and cerebral blood flow and neural function and cerebral infarction volume after cerebral ischemia-reperfusion injury in rats.Methods Twenty-seven male SD rats were divided into sham group,model group,and EA pretreatment group according to the random number table method,with 9 rats in each group.Rats in the sham group were treated as the same as the rats in the model group except for not inserting thread plug.Rats in the model group were restrained for 14 days before surgery,and the middle cerebral artery occlusion ischemia-reperfusion model was established by thread-occluded method.Rats in the EA pretreatment group were pretreated with EA 14 days before surgery,other same model groups.The cerebral blood flow rate instant after modeling,and after reperfusion,the Bederson score,mNSS score,cerebral infarction volume at 24 hours after surgery were compared.The spatial learning and memory ability was tested by the Morris water maze experiment;the level of serum HO-1 was detected by enzyme-linked immunosorbent assay.Results At instant after modeling,60,120 minutes after modeling,and 10,20,and 30 minutes after reperfusion,compared with the sham group,the cerebral blood flow of the model group rats was significantly decreased,and the differences were statistically significant(P<0.05);compared with the model group,the cerebral blood flow of rats in the EA pretreatment group was significantly increased,and the differences were statistically significant(P<0.05).At 24 hours after modeling,compared with the sham group,the Bederson score and mNSS score of the model group rats were increased,and the differences were statistically significant(P<0.05);compared with the model group,the Bederson score and mNSS score of the EA pretreatment group were decreased,and the differences were statistically significant(P<0.05).At 24 hours after modeling,there was no infarct formation in the sham group with TTC staining,while gray white infarcts of varying degrees were observed in both the model group and the EA pretreatment group.Compared with the model group,the proportion of cerebral infarction in the EA pretreatment group was significantly decreased,and the difference was statistically significant(P<0.05).There was no statistically significant difference in the percentage of fourth quadrant residence time and serum HO-1 levels between the sham group and the model group(P>0.05);compared with the model group,the percentage of fourth quadrant retention time and serum HO-1 level in the EA pretreatment group were increased,and the differences were statistically significant(P<0.05).Conclusion EA pretreatment can regulate cerebral blood flow,improve nerve defect function,reduce cerebral infarction volume,improve cognitive level and exert neuroprotective effects on cerebral ischemia-reperfusion injury.And its mechanism may be related to increasing the expression level of HO-1 protein in the serum of model rats to play an anti-oxidative stress role.