Department of Neurology, Guangdong 999 Brain Hospital, Guangzhou, China.
Laboratory Medicine, The Third Affiliated Hospital of Harbin Medical University, Harbin, China.
J Healthc Eng. 2022 Apr 13;2022:7002630. doi: 10.1155/2022/7002630. eCollection 2022.
To explore the inhibition of pramipexole on the neuronal apoptosis and its influences on the expressions of brain tissue brain-derived neurotrophic factor (BDNF), and serum miR-103a and miR-30b and inflammatory factors in rats with Parkinson's disease. A total of 36 Sprague-Dawley rats were randomly divided into normal group ( = 12), model group ( = 12) and pramipexole group ( = 12). Compared with that in normal group, the positive expression of BDNF was substantially increased in model group and pramipexole group, and its positive expression in pramipexole group was notably higher than that in model group. The WB results revealed that compared with those in normal group, the relative protein expression levels of Bax and Bcl-2 were markedly increased and decreased, respectively, in the other two groups, and that pramipexole group exhibited a remarkable decline in the relative protein expression level of Bax and a considerable increase in that of Bcl-2, compared with model group. The relative expression levels of miR-103a and miR-30b in model and pramipexole groups were markedly higher than those in normal group, and pramipexole group had remarkably higher relative expression levels of miR-103a and miR-30b than model group. It was found through ELISA that model and pramipexole groups had markedly raised IL-1 and IL-18 content compared with normal group, and their content in pramipexole group was remarkably lower than that in model group. Based on the TUNEL results, compared with that in normal group, the apoptosis rate of cells rose substantially in the other two groups, and the apoptosis rate in pramipexole group was notably lower than that in model group. Pramipexole may up-regulate the expressions of BDNF, miR-103a and miR-30b to inhibit the apoptosis and inflammation in Parkinson's disease model rats.
探讨普拉克索对神经元凋亡的抑制作用及其对帕金森病大鼠脑组织脑源性神经营养因子（BDNF）、血清 miR-103a 和 miR-30b 及炎症因子表达的影响。将 36 只 Sprague-Dawley 大鼠随机分为正常组（n=12）、模型组（n=12）和普拉克索组（n=12）。与正常组相比，模型组和普拉克索组 BDNF 的阳性表达明显增加，普拉克索组的阳性表达明显高于模型组。WB 结果显示，与正常组相比，另外两组 Bax 和 Bcl-2 的相对蛋白表达水平明显升高和降低，普拉克索组 Bax 的相对蛋白表达水平明显下降，Bcl-2 的相对蛋白表达水平明显升高，与模型组相比。模型组和普拉克索组 miR-103a 和 miR-30b 的相对表达水平明显高于正常组，普拉克索组 miR-103a 和 miR-30b 的相对表达水平明显高于模型组。ELISA 结果显示，与正常组相比，模型组和普拉克索组 IL-1 和 IL-18 含量明显升高，普拉克索组含量明显低于模型组。TUNEL 结果显示，与正常组相比，另外两组细胞凋亡率明显升高，普拉克索组细胞凋亡率明显低于模型组。普拉克索可能通过上调 BDNF、miR-103a 和 miR-30b 的表达来抑制帕金森病模型大鼠的细胞凋亡和炎症反应。
