帕金森病多巴胺细胞凋亡与Fas基因表达的机制研究

Abstract
Figure/Table
References (20)
Related Citation (15)

Download: PDF (926 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective To explore the antiapoptosis effect on dopamine cell in the rat model of Parkinson′s disease (PD) after Fas gene mRNA inhibition. Methods Seventy-five SD rats were divided into 5 groups by random number table method, with 15 rats in each group. Blank control group: normal saline was injected into the substantia nigra of rats. PD group: intracerebral injection of 6-OHDA. In Fas siRNA group: Fas gene inhibitor Fas siRNA was injected into the substantia nigra of brain, and 6-OHDA of the same amount was injected 2 days later. Positive control group and negative control group: Fas siRNA positive control and negative control were injected into the substantia nigra respectively, and 6-OHDA of the same measurement was injected 2 days later. Immunohistochemistry, PCR and Western blot were used to detect the number of dopamine positive cells, Fas mRNA and the relative expression of Fas protein. Results The number of TH positive cells in PD group was less than that in blank control group (P < 0.05). The number of TH positive cells in FAS siRNA group and positive control group was higher than that in PD group (P < 0.05). The number of TH positive cells in FAS siRNA group and positive control group was more than that in negative control group (P < 0.05). The relative expression of Fas-mRNA and Fas-protein in PD group was higher than that in blank control group (P < 0.05). The relative expression of Fas-mRNA and Fas-protein in FAS siRNA group and positive control group were lower than that in PD group (P < 0.05). The relative expression of Fas-mRNA and Fas-protein in Fas siRNA group and positive control group was lower than that in negative control group (P < 0.05). Conclusion The dopamine apoptosis can be reduced effectively after the inhibition of expression of Fas gene.

Key words： Parkinson′s disease Apoptosis Fas gene RNA inhibitio

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	XIA Huan1 LUO Qin2 WANG Yuling3 GAO Hua4 YANG Xinling5▲

Cite this article:

XIA Huan1 LUO Qin2 WANG Yuling3 GAO Hua4 YANG Xinling5▲. Study on mechanism of dopamine apoptosis and Fas gene expression in Parkinson′s disease[J]. 中国医药导报, 2019, 16(34): 4-6,30.

URL:

http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2019/V16/I34/4

[1] Cao Q，Qin L，Huang F，et al. Amentoflavone protects dopaminergic neurons in MPTP-induced Parkinson′s disease model mice through PI3K/Akt and ERK signaling pathways [J]. Toxicol Appl Pharmacol，2017，319：80-90.
[2] Chen YY，Jeffery HC，Hunter S，et al. Human intrahepatic regulatory T cells are functional，require IL-2 from effector cells for survival，and are susceptible to Fas ligand‐mediated apoptosis [J]. Hepatology，2016，64（1）：138-150.
[3] Planells-Ferrer L，Urresti J，Coccia E，et al. Fas apoptosis inhibitory molecules：more than death-receptor antagonists in the nervous system [J]. J Neurochem，2016，139（1）：11-21.
[4] 王佳慧，郑洋，王嘉孺，等.基于KEGG通路和基因网络对慢性萎缩性胃炎靶点基因的筛选[J].中国医药导报，2019，16（2）：159-163，173.
[5] Tiwari PC，Pal R. The potential role of neuroinflammation and transcription factors in Parkinson disease [J]. Dialogues Clin Neurosci，2017，19（1）：71-80.
[6] Song E，Lee SK，Wang J，et al. RNA interference targeting Fas protects mice from fulminant hepatitis [J]. Nat Med，2003，9（3）：347-351.
[7] Hamar P，Song E，K?觟kény G，et al. Small interfering RNA targeting Fas protects mice against renal ischemia-reperfusion injury [J]. Proc Natl Acad Sci USA，2004，101（41）：14883-14888.
[8] Liu J，Liu W，Lu Y，et al. Piperlongumine restores the balance of autophagy and apoptosis by increasing BCL2 phosphorylation in rotenone-induced Parkinson disease models [J]. Autophagy，2018，14（5）：845-861.
[9] Kingsbury AE，David Mardsen C，Foster OJF. DNA fragmentation in human substantia nigra：apoptosis or perimortem effect? [J]. Mov Disord，1998，13（6）：877-884.
[10] Martinez BA，Petersen DA，Gaeta AL，et al. Dysregulation of the mitochondrial unfolded protein response induces non-apoptotic dopaminergic neurodegeneration in C. elegans models of Parkinson′s disease [J]. J Neurosci，2017，37（46）：11085-11100.
[11] Jabir NR，Firoz CK，Baeesa SS，et al. Synopsis on the linkage of Alzheimer′s and Parkinson′s disease with chronic diseases [J]. CNS Neurosci，2015，21（1）：1-7.
[12] Bose A，Beal MF. Mitochondrial dysfunction in Parkinson′s disease [J]. Neurochem，2016，139（Suppl 1）：216-231.
[13] Zhang J，Shi L，Zhang L，et al. MicroRNA-25 negatively regulates cerebral ischemia/reperfusion injury-induced cell apoptosis through Fas/FasL pathway [J]. J Mol Neurosci，2016，58（4）：507-516.
[14] Feng J，Feng L，Zhang G. Mitochondrial damage in hippocampal neurons of rats with epileptic protein expression of Fas and caspase-3 [J]. Exp Ther Med，2018，16（3）：2483-2489.
[15] Guiney SJ，Adlard PA，Bush AI，et al. Ferroptosis and cell death mechanisms in Parkinson′s disease [J]. Neurochem Int，2017，104：34-48.
[16] Yuan F，Xia H. Study on changes of Fas，p-BAD and caspase-8 expression in acute myocardial infarction rats treated by Guanxin decoction [J]. Biomed Res，2017，28（21）：9225-9230.
[17] Jiang M，Yun Q，Niu G，et al. Puerarin prevents inflammation and apoptosis in the neurocytes of a murine Parkinson′s disease model [J]. Genet Mol Res，2016，15（4）：1-9.
[18] Ferrer I，Blanco R，Cutillas B，et al. Fas and Fas-L expression in Huntington′s disease and Parkinson′s disease [J]. Neuropathol Appl Neurobiol，2000，26（5）：424-433.
[19] Komnig D，Schulz JB，Reich A，et al. Mice lacking Faim2 show increased cell death in the MPTP mouse model of Parkinson disease [J]. J Neurochem，2016，139（5）：848-857.
[20] Jiang MJ，Chen YH，Li L，et al. Protective effects of DL-3-n-butylphthalide in the lipopolysaccharide-induced mouse model of Parkinson′s disease [J]. Mol Med Rep，2017，16（5）：6184-6189.