Abstract:【Objective】To observe the effect of sodium selenite on the morphology of the substantia nigra and the content of glutamate in the striatum of Parkinson's disease (PD) rats, and to explore the related mechanisms. 【Methods】A PD rat model was established by injecting 6-Hydroxydopamine (6-OHDA). Twenty successfully modeled rats were randomly divided into the model group and the experimental group, with 10 rats in each group. Ten rats were injected with saline only and set as the control group. Fifteen days after the injection, the experimental group were given sodium selenite 100 mg/kg, while the control group and model group were given an equal volume of normal saline, once a day for 30 consecutive days. The cognitive function was detected by T-maze experiment. The content of glutamate in the striatum were detected by high performance liquid chromatography (HPLC). The relative expression of substantia nigra c-Jun N-terminal kinase (JNK) and p-JNK protein were detected by Western blotting. 【Results】The accuracy rates of the T-maze experiment in the control group, the model group and the experimental group were (94.44±5.27)%, (50.00±6.39)% and (72.22±8.42)%, respectively. Of which, the content of glutamate in the striatum were (15.96±2.79)μg/mL, (31.87±4.21)μg/mL and (23.34±3.92)μg/mL. The substantia nigra p-JNK/JNK in the control group, the model group and the experimental group were 0.19±0.02,0.78±0.08 and 0.27±0.03, respectively. The differences of the correct rate of T-maze experiment, striatal glutamate content, substantia nigra p-JNK/JNK ratio between the model group and the control group were statistically significant (P<0.05). They were also significant differences between the model group and the experimental group(P<0.05). 【Conclusion】Sodium selenite can improve the cognitive function of PD rats in terms of the morphology of substantia nigra neurons, protect the function of substantia nigra dopaminergic neurons, and reduce the content of striatal glutamate, which may be achieved by inhibiting the JNK signaling pathway.
范凯. 亚硒酸钠对帕金森病大鼠黑质形态学及纹状体谷氨酸含量的影响及机制研究[J]. 医学临床研究, 2022, 39(2): 236-239.
FAN Kai. Effect of Sodium Selenite on the Morphology of the Substantia Nigra and the Content of Glutamate in the Striatum of Rats with Parkinson's Disease. JOURNAL OF CLINICAL RESEARCH, 2022, 39(2): 236-239.
[1] SIMON D K, TANNER C M, BRUNDIN P. Parkinson Disease Epidemiology, Pathology, Genetics, and Pathophysiology[J].Clin Geriatr Med,2020, 36(1):1-12.
[2] IOVINO L, TREMBLAY M E, CIVIERO L. Glutamate-induced excitotoxicity in Parkinson's disease: The role of glial cells[J].J Pharmacol Sci,2020, 144(3):151-164.
[3] 贾敏, 易继涛, 王从平, 等. 帕金森患者细胞因子, 微量元素及抗氧化酶水平变化[J].临床军医杂志, 2019, 47(8):44-45.
[4] 张思妍, 王宝, 陶凯, 等. 帕金森病大鼠模型的建立及超声影像评价[J].中华超声影像学杂志, 2020, 29(6):540-544.
[5] QI Y H, ZHU R, WANG Q, et al. Early intervention with gastrodin reduces striatal neurotoxicity in adult rats with experimentally induced diabetes mellitus[J].Mol Med Rep,2019, 19(4):3114-3122.
[6] BALESTRINO R, SCHAPIRA A H V. Parkinson disease[J].Eur J Neurol,2020, 27(1):27-42.
[7] NAGATSU T, NAKASHIMA A, ICHINOSE H, et al. Human tyrosine hydroxylase in Parkinson's disease and in related disorders[J].J Neural Transm (Vienna),2019, 126(4):397-409.
[8] COLLE D, SANTOS DB, DE SOUZA V, et al. Sodium selenite protects from 3-nitropropionic acid-induced oxidative stress in cultured primary cortical neurons[J].Mol Biol Rep,2019, 46(1):751-762.
[9] ZHAO X H, WANG Y B, YANG J, et al. MicroRNA-326 suppresses iNOS expression and promotes autophagy of dopaminergic neurons through the JNK signaling by targeting XBP1 in a mouse model of Parkinson's disease[J].J Cell Biochem,2019, 120(9):14995-15006.