SNP-9对鱼藤酮所致帕金森病细胞模型的作用及机制研究

黄志欢; 梁潇; 高向东; 陈松

doi:10.11665/j.issn.1000-5048.2023020101

SNP-9对鱼藤酮所致帕金森病细胞模型的作用及机制研究

中国药科大学生命科学与技术学院江苏省生物药物成药性研究重点实验室，南京 211198

基金项目: 国家自然科学基金资助项目（No.82073755；No.82173728）；国家级大学生创新创业训练计划项目

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- 收稿日期: 2023-01-31
- 修回日期: 2023-03-20
- 刊出日期: 2023-04-24

Effects and mechanisms of SNP-9 on Parkinson''s disease cell model induced by rotenone

Jiangsu Provincial Key Laboratory of Druggability of Biopharmaceuticals, School of Life Science and Technology, China Pharmaceutical University, Nanjing 211198, China

Funds: This study was supported by the National Natural Science Foundation of China (No. 82073755, No. 82173728); and the National Innovation and Entrepreneurship Training Program for Undergraduate

摘要

摘要: 本文研究SNP-9对帕金森病（Parkinson’s disease， PD）细胞模型的作用和机制。使用鱼藤酮损伤SH-SY5Y细胞建立PD细胞模型；通过MTT法检测鱼藤酮和SNP-9对细胞活力的影响；Hoechst/PI双染法检测鱼藤酮和SNP-9对细胞凋亡的影响；DCFH-DA探针检测鱼藤酮和SNP-9对细胞活性氧（reactive oxygen species， ROS）水平的影响；Western blot检测鱼藤酮和SNP-9对酪氨酸羟化酶（tyrosine hydroxylase， TH）、α-突触核蛋白（α-synuclein， α-syn）、Bcl-2、Bax蛋白水平的影响。研究结果显示，SNP-9能够缓解鱼藤酮诱导的SH-SY5Y细胞活力、TH和α-syn水平、细胞凋亡、ROS水平，以及细胞凋亡相关蛋白Bax/Bcl-2的异常。研究结果提示SNP-9可能通过调控凋亡相关通路，进而缓解鱼藤酮导致的神经细胞损伤。
- 帕金森病 /
- SNP-9 /
- 鱼藤酮 /
- 凋亡
Abstract: In this article, the effects and mechanisms of SNP-9 on Parkinson''s disease (PD) cell model were investigated.SH-SY5Y cells were treated with rotenone to establish PD cell model; the effects of rotenone and SNP-9 on cell viability were detected by MTT assay; Hoechst/PI double staining assay was used to detect the effects of rotenone and SNP-9 on cell apoptosis; DCFH-DA probe was used to detect the effects of rotenone and SNP-9 on cellular reactive oxygen species (ROS) levels; and Western blot was used to detect the effects of rotenone and SNP-9 on protein levels of tyrosine hydroxylase (TH), α-synuclein (α-syn), Bcl-2 and Bax.The results showed that SNP-9 could alleviate abnormalities in cell viability, levels of TH and α-syn, apoptosis, ROS and apoptotic relative protein Bax/Bcl-2 induced by rotenone.Our findings suggest that SNP-9 may alleviate rotenone-induced injury in neuronal cells by regulating cell apoptosis related pathway.
- Parkinson''s disease /
- SNP-9 /
- rotenone /
- apoptosis

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参考文献(21)

[1]	Panicker N, Kam TI, Wang H, et al. Neuronal NLRP3 is a parkin substrate that drives neurodegeneration in Parkinson''s disease[J]. Neuron, 2022, 110(15): 2422-2437.e9.
[2]	Mahul-Mellier AL, Burtscher J, Maharjan N, et al. The process of Lewy body formation, rather than simply α-synuclein fibrillization, is one of the major drivers of neurodegeneration[J]. Proc Natl Acad Sci U S A, 2020, 117(9): 4971-4982.
[3]	Davie CA. A review of Parkinson''s disease[J]. Br Med Bull, 2008, 86: 109-127.
[4]	Mantovani S, Smith SS, Gordon R, et al. An overview of sleep and circadian dysfunction in Parkinson''s disease[J]. J Sleep Res, 2018, 27(3): e12673.
[5]	Hussein A, Guevara CA, Del Valle P, et al. Non-motor symptoms of Parkinson''s disease: the neurobiology of early psychiatric and cognitive dysfunction[J]. Neuroscientist, 2023, 29(1): 97-116.
[6]	Jankovic J,Tan EK. Parkinson''s disease: etiopathogenesis and treatment[J]. J Neurol Neurosurg Psychiatry, 2020, 91(8): 795-808.
[7]	Bloem BR, Okun MS, Klein C. Parkinson''s disease[J]. Lancet, 2021, 397(10291): 2284-2303.
[8]	Yao S, Xu Z, Chen S, et al. Silk fibroin hydrolysate improves memory impairment via multi-target function[J]. J Funct Foods, 2022, 89: 104942.
[9]	Xu Z, Chen S, Wang Y, et al. Neuroprotective effects of silk fibroin hydrolysate against Aβ_25–35 induced cytotoxicity in SH-SY5Y cells and primary hippocampal neurons by regulating ROS inactivation of PP2A[J]. J Funct Foods, 2018, 45: 100-109.
[10]	Zaman V, Shields DC, Shams R, et al. Cellular and molecular pathophysiology in the progression of Parkinson''s disease[J]. Metab Brain Dis, 2021, 36(5): 815-827.
[11]	Subramaniam SR, Chesselet MF. Mitochondrial dysfunction and oxidative stress in Parkinson''s disease[J]. Prog Neurobiol, 2013, 106-107: 17-32.
[12]	Trist BG, Hare DJ, Double KL. Oxidative stress in the aging substantia nigra and the etiology of Parkinson''s disease[J]. Aging Cell, 2019, 18(6): e13031.
[13]	Ott M, Gogvadze V, Orrenius S, et al. Mitochondria, oxidative stress and cell death[J]. Apoptosis, 2007, 12(5): 913-922.
[14]	Rocha SM, Bantle CM, Aboellail T, et al. Rotenone induces regionally distinct α-synuclein protein aggregation and activation of glia prior to loss of dopaminergic neurons in C57Bl/6 mice[J]. Neurobiol Dis, 2022, 167: 105685.
[15]	Radad K, Al-Shraim M, Al-Emam A, et al. Rotenone: from modelling to implication in Parkinson''s disease[J]. Folia Neuropathol, 2019, 57(4): 317-326.
[16]	Chen YJ, Gao XD, Chen S. Effects and mechanisms of FGF21 on neuronal damage induced by rotenone[J]. J China Pharm Univ (中国药科大学学报),2020,51(6):718-723.
[17]	Zha Q, Gao XD, Chen S. Effects of VHL inhibitor on rotenone-induced Caenorhabditis elegans model of Parkinson''s disease[J]. J China Pharm Univ (中国药科大学学报), 2021, 52(3): 346-351.
[18]	Lopes FM, da Motta LL, De Bastiani MA, et al. RA differentiation enhances dopaminergic features, changes redox parameters, and increases dopamine transporter dependency in 6-Hydroxydopamine-induced neurotoxicity in SH-SY5Y cells[J]. Neurotox Res, 2017, 31(4): 545-559.
[19]	Lopes FM, Schr?der R, da Frota ML, Jr., et al. Comparison between proliferative and neuron-like SH-SY5Y cells as an in vitro model for Parkinson disease studies[J]. Brain Res, 2010, 1337: 85-94.
[20]	Dionísio PA, Amaral JD, Rodrigues CMP. Oxidative stress and regulated cell death in Parkinson''s disease[J]. Ageing Res Rev, 2021, 67: 101263.
[21]	Wu Y, Chen M, Jiang J. Mitochondrial dysfunction in neurodegenerative diseases and drug targets via apoptotic signaling[J]. Mitochondrion, 2019, 49: 35-45.

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SNP-9对鱼藤酮所致帕金森病细胞模型的作用及机制研究

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Effects and mechanisms of SNP-9 on Parkinson''s disease cell model induced by rotenone

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