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| Study on SPTLC2 expression level in brain tissue in the rat model of Parkinson disease |
| HE Xiaoyan JIAO Yan LI Hongyan |
| Department of Neurology, People's Hospital of Xinjiang Uygur Autonomous Region, Xinjiang Uygur Autonomous Region, Urumqi 830001, China |
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Abstract Objective To explore the expression of serine palmitate transferase long chain subunit 2 (SPTLC2) in brain tissue in the rat model of Parkinson disease. Methods Parkinson rat model was prepared by injecting 6-hydroxy dopamine, and the rats were divided into three groups, 2-week model group, 4-week model group, 8-week model group, and normal group. Behaviors of rats in each group were assessed by using abnormal involuntary movement (AIM) scoring method. Rotation duration, starting time, the cycle number of agent peak were recorded meanwhile. HE staining method was used to observe the changes of brain tissue in rats, and the expression of α synuclein in rat brain tissue was detected by immunohistochemistry, and SPTLC2 and mRNA expression in brain tissue of rats was detected by using RT-PCR, and SPTLC2 protein expression in rat brain tissue was detected by Western blot. Results AIM score, rotation duration, starting time, agent peak rotation number in model group was higher than those in the normal group, and with the extension of time, AIM score, rotating start time, agent peak rotation number gradually increased, while the rotation starting time gradually decreased, with statistically significant differences (P ＜ 0.05). Immunohistochemical staining showed that the number of positive cells in the normal group was less than that in the normal group, and the number of positive cells in the model group increased significantly. The number of positive cells increased gradually with the extension of time. Compared with those in the normal group and 2-week model group, SPTLC2 gene and protein expression in 4-week and 8-week model group increased, and compared with 4-week model group, SPTLC2 gene and protein expression in 8-week model group increased, with statistically significant differences (P ＜ 0.05). Conclusion SPTLC2 may be involved in the pathogenesis of Parkinson disease, via up-regulating SPTLC2 gene and protein expression.
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[1] 张雪，张雯，杜立达，等.抗帕金森病病药物及其作用靶点研究进展[J].国际药学研究杂志，2016，43（1）：87-96.
[2] Nicholson.常染色体显性遗传性感觉神经病变伴慢性咳嗽和胃食管反流：2个染色体3p22-p24相关家族的临床特征[J].世界核心医学期刊文摘：神经病学分册，2006， 24（6）：54-54.
[3] 陈旭，耿翔.帕金森病病发病机制新进展[J].中华老年心脑血管病杂志，2014，16（9）：897-898.
[4] Early M，Wink L，Erickson C，et al. Abnormal Involuntary Movement Scale [J]. Schizophr Res. 2005，77（2/3）：119-128.
[5] 李晓霞.锰与帕金森病病发病机制的相关研究[J].成都医学院学报，2013，8（6）：720-723.
[6] Drake JD，Kibuuka LN，Dimitrov KD，et al. Abnormal involuntary movement（AIM）expression following D2 dopamine agonist challenge is determined by the nature of prior dopamine receptor stimulation（priming）in 6-hydroxydopamine lesioned rats [J]. Pharmacol Biochem Behav，2013， 105（12）：26-33.
[7] 孙涛.帕金森病病实验动物模型的研究进展[J].中国新药杂志，2014，23（18）：2155-2160.
[8] 魏翔，刘晓莉.帕金森病病大鼠模型运动行为测评方法的研究进展[J].中国实验动物学报，2015，23（2）：209-215.
[9] Ho SC，Hsu CC，Pawlak CR，et al. Effects of ceftriaxone on the behavioral and neuronal changes in an MPTP-induced Parkinson's disease rat model [J]. Behav Brain Res，2014，15（268）：177-184. Doi：10.1016/j.bbr.2014.04.022.
[10] Tran HT，Chung CH，Iba M，et al. A-synuclein immunotherapy blocks uptake and templated propagation of misfolded α-synuclein and neurodegeneration [J]. Cell Rep，2014，7（6）：2054-2065.
[11] Dettmer U，Newman AJ，Luth ES，et al. In Vivo Cross-linking Reveals Principally Oligomeric Forms of α-Synuclein and β-Synuclein in Neurons and Non-neural Cells [J]. J Biol Chem，2013，288（9）：6371-6385.
[12] Wang X，Chen Q，Xing D. Focal adhesion kinase activates NF-κB via the ERK1/2 and p38MAPK Pathways in amyloid-β25-35-induced apoptosis in PC12 cells [J]. J Alzheimers Dis，2012，32（1）：77-81.
[13] 楼彩霞.髓系细胞特异性Sptlc2基因缺失对小鼠动脉粥样硬化病灶的影响[D].北京：中央民族大学，2013.
[14] Suriyanarayanan S，Auranen M，Toppila J，et al. The Variant p.（Arg183Trp）in SPTLC2 Causes Late-Onset Hereditary Sensory Neuropathy [J]. Neuromolecular Med，2016， 18（1）：81-85.
[15] Lee SY，Kim JR，Hu Y，et al. Cardiomyocyte specific deficiency of serine palmitoyltransferase subunit 2 reduces ceramide but leads to cardiac dysfunction [J]. J Bio Chem，2012，287（22）：18429-18433.
[16] 刘青.SPT抑制剂多球壳菌素对油酸诱导的HSC凋亡及自噬的影响[D].衡阳：南华大学，2016. |
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