Physiology Division, Department of Basic Science, School of Veterinary Medicine, Shiraz University, Shiraz, Iran.
Department of Pathobiology, School of Veterinary Medicine, Shiraz University, Shiraz, Iran.
Biomed Res Int. 2020 May 1;2020:2546365. doi: 10.1155/2020/2546365. eCollection 2020.
Parkinson's disease (PD) is a neurodegenerative disorder with progressive motor defects. Therefore, the aim of the present investigation was to examine whether catalepsy, asymmetry, and nociceptive behaviors; the Nissl-body and neuron distribution; brain-derived neurotrophic factor (BDNF); malondialdehyde (MDA); total antioxidant capacity (TAC) levels; and the percentage of dopamine depletion of striatal neurons in the rat model of Parkinson's disease (PD) can be affected by (TG) infection.
Fifty rats were divided into five groups: control (intact rats), sham (rats which received an intrastriatal injection of artificial cerebrospinal fluid (ACSF)), PD control (induction of PD without TG infection), TG control (rats infected by TG without PD induction), and PD infected (third week after PD induction, infection by TG was done). PD was induced by the unilateral intrastriatal microinjection of 6-hydroxydopamine (6-OHDA) and ELISA quantified dopamine, BDNF, MDA, and TAC in the striatum tissue. Cataleptic, asymmetrical, nociceptive, and histological alterations were determined by bar test, elevated body swing test, formalin test, and Nissl-body and neuron counting in the striatal neurons.
The results demonstrated that PD could significantly increase the number of biased swings, descent latency time, and nociceptive behavior and decrease the distribution of Nissl-stained neurons compared to the control and sham groups. TG infection significantly improved biased swing, descent latency time, nociceptive behavior, and the Nissl-body distribution in striatal neurons in comparison to the PD control group. The striatal level of BDNF in the PD-infected and TG control groups significantly increased relative to the PD control group. The striatal MDA was significantly higher in the PD control than other groups, while striatal TAC was significantly lower in the PD control than other groups.
The current study indicates that TG infection could improve the cataleptic, asymmetric, nociceptive and behaviors; the level of striatal dopamine release; BDNF levels; TAC; and MDA in PD rats.
帕金森病（PD）是一种进行性运动缺陷的神经退行性疾病。因此，本研究旨在探讨是否可以通过（TG）感染来影响帕金森病（PD）大鼠模型的僵住、不对称和痛觉行为；尼氏体和神经元分布；脑源性神经营养因子（BDNF）；丙二醛（MDA）；总抗氧化能力（TAC）水平；以及纹状体神经元中多巴胺的耗竭百分比。
将 50 只大鼠分为五组：对照组（完整大鼠）、假手术组（接受纹状体内人工脑脊液（ACSF）注射的大鼠）、PD 对照组（无 TG 感染诱导的 PD）、TG 对照组（无 PD 诱导感染的 TG）和 PD 感染组（PD 诱导后第三周进行 TG 感染）。通过单侧纹状体内微量注射 6-羟多巴胺（6-OHDA）诱导 PD，通过酶联免疫吸附试验（ELISA）测定纹状体组织中的多巴胺、BDNF、MDA 和 TAC。通过棒测试确定僵住、不对称、痛觉和组织学改变，通过高架体摆动测试、福尔马林测试和纹状体神经元尼氏体和神经元计数确定偏侧摆动、下降潜伏期时间和痛觉行为。
结果表明，与对照组和假手术组相比，PD 可显著增加偏侧摆动次数、下降潜伏期时间和痛觉行为，并减少纹状体神经元尼氏体的分布。与 PD 对照组相比，TG 感染可显著改善偏侧摆动、下降潜伏期时间、痛觉行为和纹状体神经元尼氏体的分布。与 PD 对照组相比，PD 感染和 TG 对照组的纹状体 BDNF 水平显著增加。与其他组相比，PD 对照组纹状体 MDA 水平显著升高，而 PD 对照组纹状体 TAC 水平显著降低。
本研究表明，TG 感染可改善 PD 大鼠的僵住、不对称、痛觉和行为；纹状体多巴胺释放水平；BDNF 水平；TAC；和 MDA。
