摘要
目的明确6-羟基多巴(6-OHDA)致多巴胺能神经元凋亡与氧化应激的关系,以及外源性超氧化物歧化酶(SOD)对多巴胺能神经元凋亡的保护作用。方法大鼠随机分组,检测大鼠的行为学变化、中脑活性氧水平,并观察大鼠中脑黑质部位TH阳性细胞和细胞凋亡的情况。结果6-OHDA注入黑质区后,活性氧升高至129.82±16.79(u/mgprot);外源性SOD有效降低活性氧水平,大鼠右侧中脑黑质区TH阳性细胞数明显增多,而凋亡细胞有所减少,大鼠的旋转圈数也明显降低。结论氧化应激在6-OH-DA致大鼠中脑多巴胺能神经元凋亡的过程中,起一定的作用;而外源性SOD增强了对活性氧的灭活能力,减弱了6-OHDA的神经毒作用,提高了多巴胺能神经元的存活,改善了大鼠的旋转行为。
Objective To define oxidative stress and antagonistic action of the exogenous SOD in the apoptosis of the rat midbrain dopaminergic neuronal induced by 6-OHDA.Method Measurement the midbrain active oxygen, the action changes and the changes of TH immunoreactive positive and apoptosis cells in SNc of each groups.Result Active oxygen in midbrain increased remarkablely (129.82±16.79 u/mgprot) after 6-OHDA injected into SNc.Otherwise,after injected exogenous SOD,the rotational speeds receded and active oxygen decreased remarkablely(P< 0.05),TH immunoreactive positive and apoptosis cells in SNc respondly changed.Conclusion Oxidative stress played a main role in apoptosis of doparminerigic neuron by injected 6-OHDA into SNc.Moreover,exogenous SOD in SNc effectively reduced active oxygen, which promoted the ability to anti-neurotoxin of doparminergic neuron, reduced doparminergic neuron apoptosis and ameliorated the rat rotating behavior.
出处
《中国组织工程研究与临床康复》
CAS
CSCD
2001年第22期54-55,57,共3页
Journal of Clinical Rehabilitative Tissue Engineering Research
基金
广东省科技厅重大科技团队项目基金粤科基办(2000)25
