Background

Parkinson's disease (PD) is a common degenerative disease of the central nervous system in the elderly. In recent years, the results of clinical and experimental studies have shown that oxidative stress is one of the important pathogenesis of PD. Selenium is one of the minor elements reported to possess antioxidant properties. Thus, the purpose of this study was to investigate the recovery effect of glycine nano-selenium on neurobehavioral abnormalities and oxidative stress caused by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in rat.

Materials and methods

SD male rats weighing 280−310 g were purchased from the Chengdu Dossy Experimental Animals Company, China. All rats were housed in a temperature-controlled room, with a 12 h light–dark cycles and had free access to food and water ad libitum. Rats were randomly divided into 4 groups with 8 animals in each group: the control group (normal saline), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine group (MPTP), MPTP + 0.05 mg/kg glycine nano-selenium (MPTP + 0.05 Se), MPTP + 0.1 mg/kg glycine nano-selenium (MPTP + 0.1 Se). Behavioral assessment, clinical symptoms, Immunohistochemistry analysis of tyrosine hydroxylase (TH) and antioxidant activity were accessed to determine the protective effects glycine nano-selenium have on PD rats.

Results

From the results, Rats showed a decrease in spontaneous motor behavior and an increase in pole test score. Also, the number of TH⁺ neurons were also significantly decreased (P < 0.05) after treated with MPTP for 7 days indicating that MPTP could successfully induce neurobehavioral abnormalities in rats. Furthermore, the lipid peroxide (MDA) levels of the PD model group were significantly increased and the antioxidant activities (SOD and GSH-PX) were significantly inhibited (P < 0.05) compared to the control group indicating the important role oxidative stress played in dopaminergic neuron death and neurobehavioral abnormalities in PD rats. Compared with the PD model group, glycine nano-selenium administration could significantly improve behavior and increase the number of TH⁺ neurons (P < 0.05) to protect against the loss of dopaminergic neurons. At the same time, glycine nano-selenium could decrease the MDA levels and increase the activities of SOD and GSH-PX significantly (P < 0.05).

Conclusion

In conclusion, PD rat model was successfully developed by intraperitoneal injection of MPTP and the intragastric administration of glycine nano-selenium reduced neurobehavioral abnormalities by decreasing oxidative stress in rat brain.

中文翻译：

---

甘氨酸纳米硒可预防由 MPTP 引起的大鼠脑氧化应激和神经行为异常

背景

帕金森病（PD）是一种常见的中老年人中枢神经系统退行性疾病。近年来的临床和实验研究结果表明，氧化应激是PD的重要发病机制之一。硒是据报道具有抗氧化特性的微量元素之一。因此，本研究的目的是研究甘氨酸纳米硒对1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）引起的大鼠神经行为异常和氧化应激的恢复作用。

材料和方法

SD 雄性大鼠，体重 280~310 g，购自成都多西实验动物公司。所有大鼠都被安置在一个温度控制的房间里，有 12 小时的明暗循环，并且可以自由进食和饮水。大鼠随机分为4组，每组8只：对照组（生理盐水），1-甲基-4-苯基-1,2,3,6-四氢吡啶组（MPTP），MPTP+0.05 mg/kg甘氨酸纳米硒（MPTP + 0.05 Se），MPTP + 0.1 mg/kg 甘氨酸纳米硒（MPTP + 0.1 Se）。通过行为评估、临床症状、酪氨酸羟化酶 (TH) 的免疫组织化学分析和抗氧化活性，确定甘氨酸纳米硒对 PD 大鼠的保护作用。

结果

从结果来看，大鼠表现出自发运动行为的减少和杆测试分数的增加。此外， 用 MPTP 处理 7 天后TH ⁺神经元的数量也显着减少（P < 0.05），表明 MPTP 可以成功诱导大鼠的神经行为异常。此外，PD模型组脂质过氧化物（MDA）水平显着升高，抗氧化活性（SOD和GSH-PX）显着受到抑制（P < 0.05) 与对照组相比，表明氧化应激在 PD 大鼠的多巴胺能神经元死亡和神经行为异常中起重要作用。与PD模型组相比，甘氨酸纳米硒给药可显着改善行为并增加TH ⁺神经元数量（P  < 0.05），以防止多巴胺能神经元的丢失。同时甘氨酸纳米硒可显着降低MDA水平，显着提高SOD和GSH-PX的活性（P  < 0.05）。

结论

综上所述，通过腹腔注射 MPTP 成功建立了 PD 大鼠模型，甘氨酸纳米硒灌胃给药可通过降低大鼠大脑的氧化应激减少神经行为异常。