论文部分内容阅读
目的:研究早期帕金森病(PD)大鼠脑内凋亡因子的改变及蝎源活性肽的保护作用。方法:选取健康雄性SD大鼠,体重为180~220 g,随机分为4组(n=10):早期PD模型组、假手术对照组、单独蝎源活性肽处理组和蝎源活性肽治疗组。采用6羟多巴胺(6-OHDA)制备大鼠PD早期模型,免疫组化观察大鼠黑质致密部和纹状体尾状核处Bax和Bcl-2免疫反应阳性颗粒数量和光密度的变化,观察大鼠PD发病早期脑内促进凋亡的Bax和抑制凋亡的Bcl-2的表达情况,进一步观察蝎源活性肽保护作用的抗凋亡机制。结果:发现在6-OHDA给药侧,PD早期大鼠与对照组相比,脑内促进凋亡的Bax表达增强,而抑制凋亡的Bcl-2表达减弱,而蝎源活性肽可有效的逆转这种异常的表达。结论:早期PD大鼠促进凋亡的Bax表达增强和抑制凋亡的Bcl-2表达减弱参与PD的早期病变,而抗凋亡机制参与了蝎源活性肽对中脑多巴胺能神经元的早期保护作用。
Objective: To study the changes of brain apoptotic factor in the early stage of Parkinson’s disease (PD) and the protective effect of scorpion active peptides. Methods: Healthy male SD rats weighing 180-220 g were randomly divided into 4 groups (n = 10): early PD model group, sham operation control group, single scorpion active peptide treatment group and scorpion active peptide treatment group. An early model of PD was established by 6-hydroxydopamine (6-OHDA) in rats. The changes of Bax and Bcl-2 immunoreactive granules and optical density in substantia nigra pars compacta and caudate nucleus were observed by immunohistochemistry. The expression of Bcl-2 and Bcl-2 in the early stage of PD in rats and the protective effect of scorpion active peptides were further observed. Results: In the 6-OHDA administration group, the expression of Bax in the brain increased and the expression of Bcl-2 in the brain decreased compared with the control group, while the scorpion active peptide could be effective Reverse this abnormal expression. CONCLUSION: The early apoptotic Bax expression is upregulated in PD rats and the decreased expression of Bcl-2 is involved in the early lesions of PD. The anti-apoptotic mechanism is involved in the early protection of midbrain dopaminergic neurons by scorpion active peptides effect.