摘要
目的探讨糖尿病大鼠局灶性脑缺血再灌注模型中脑源性神经营养因子(BDNF)的表达及阻断泛素蛋白酶体途径(UPP)对它的影响。方法将SD大鼠随机分成正常对照组(A组)、假手术组(B组)、非糖尿病组(C组)、糖尿病组(D组)和糖尿病治疗组(E组),免疫组织化学方法观察再灌注3h、6h、24h、48h及阻断UPP后脑组织中BDNF的动态变化。结果脑缺血再灌注后,各脑梗死组BDNF表达均增加,24h达高峰,48h后下降;UPP阻断后E组脑组织中BDNF阳性细胞计数较C组、D组明显增加(P<0.05)。结论UPP阻断可通过促进内源性BDNF表达产生神经保护作用。
Objective To study the expression of brain-derived neurotrophic factor(BDNF)in focal cerebral ischemin of diabertic rat modle and the impact of blooking ubiquitin proteasome pathway (UPP). Methods Sprague-Dawley rats were randomly divided into control group (group A), sham operation group(group B ), non-diabetes cerebral infarction group(group C ),diabetes cerebral infarction group(group D )and diabetes cerebral infarction treatment group(group E),and we observed the expression variation of BDNF at 3h,6h,24h and 48h and blooking UPP after reperfusion by immunohistochemistry. Results The BDNF expression was increased in every group after ischemic and reperfusion and peaked at 24h and descented at 48h. The brain positive cell count in the group E was increased than that in the group D(P〈 0.05) after blooking UPP. Conclusion Blocking UPP can produce neuroproctection by promoting the endogenous expression of BDNF.
出处
《中国现代医生》
2009年第27期1-3,F0003,共4页
China Modern Doctor
关键词
脑缺血再灌注
UPP
BDNF
神经保护
Cerebral ischemia-reperfusion
Blooking ubiquitin proteasome pathway
Brain-derived neurotrophic factor
Neuroproctection