摘要
目的:研究大鼠局灶性脑缺血再灌注后脑组织腺苷含量、烯醇化酶表达的动态变化及桂哌齐特对此的影响。方法:采用大鼠局灶性脑缺血再灌注模型。应用反相离子对高效液相色谱法和免疫组织化学法分别检测脑腺苷含量及烯醇化酶表达的动态变化。并进行神经功能评分。结果:模型组大鼠脑缺血及再灌注后4个时间点脑腺苷含量均较基础水平(1.01±0.14)μmol/g增高(P<0.05);桂哌齐特组缺血后20min为(3.26±0.30)μmol/g,60min时为(1.91±0.20)μmol/g,较模型组犤分别为(2.40±0.38)μmol/g,F=92.572,P<0.05;(1.27±0.17)μmol/g犦显著升高(F=92.572,43.051,P<0.05),再灌注后15min及60min呈现增高的趋势(P>0.05)。烯醇化酶的表达在脑缺血再灌注后各时间点均明显降低(P<0.05),桂哌齐特组均明显高于模型组(P<0.05),且神经功能评分有明显改善。结论:脑缺血再灌注后脑组织腺苷含量急骤升高,但持续时间短暂。桂哌齐特对大鼠局灶性脑缺血再灌注损伤神经元有保护作用,可能与其增加内源性腺苷含量从而增强腺苷的脑保护作用有关。
AIM:To investigate the dynamic changes of adenosine(ADO) content and neuron specific enolase(NSE) protein expression in the brain of rats after focal cerebral ischemic reperfusion and the influence of cinepazide on them. METHODS:Animal models of focal cerebral ischemic reperfusion were established in rats.High performance liquid chromatograpy(HPLC) and immunohistochemical method were used to the dynamic changes in the content of ADO and the level of NSE protein expression,respectively.Neurological function was assayed in the rats. RESULTS:The contents of ADO in the model group were higher at four time points after ischemic reperfusion as compared with the normal level[(1.01±0.14) μmol/g,P< 0.05].As compared with the model group[(2.40±0.38) and(1.27±0.17) μmol/g],the contents of ADO in the cinepazide group[(3.26±0.30) and(1.91±0.20) μmol/g,repsectively]were significantly increased at 20 and 60 minutes after ischemia(F=92.572, 43.051,P< 0.05).Although there was no significant difference(P >0.05),the content of ADO in the cinepazide group had a slight tendency to increase 15 and 60 minutes after reperfusion.The levels of NSE expression decreased significantly at different time points after ischemic reperfusion(P< 0.05),but the level in the cinepazide was higher than that in the model group(P< 0.05).The neurological dysfunctions were all significantly improved. CONCLUSION:The contents of ADO sharply increased in the brain after focal cerebral ischemic reperfusion,but it only lasted a short time. Cinepazide plays a protective role in neurons against focal cerebral ischemic reperfusion,which may be related to its protective effect on brain by increasing the contents of endogenous ADO.
出处
《中国临床康复》
CSCD
2004年第10期1863-1865,T002,共4页
Chinese Journal of Clinical Rehabilitation
