褐藻多糖硫酸酯对MPP+损伤的MN9D细胞氧化应激及凋亡的保护作用

Abstract
Figure/Table
References (21)
Related Citation (15)

Download: PDF (782 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective To explore the protective effect of fucoidan (FUC) on the cell model of Parkinson′s disease (PD) and its mechanism. Methods PD model was established by MN9D cells which were damaged by 100 μmol/L MPP+. The cell viability of PD cell model was detected by MTS after FUC pretreatment. The reactive oxygen species (ROS) was measured by fluorescence detection, the activity of Caspase-3 in cells was measured by luciferase, the expression changes of apoptosis-related proteins Bax and Bcl-2 were measured by Western blot. Results After application of 12 h, FUC 100 μmol/L significantly increased the cell viability of MN9D cells damaged by MPP+, the difference was highly statistically significant (P ＜ 0.01). The FUC pretreatment reduced the activity of intracellular ROS of MN9D cell damaged by MPP+ in 3 h and the expression of Caspase-3 in 6 h, there were highly statistically significant differences (P ＜ 0.01). After FUC and Selegiline pretreatment, the expression of MN9D cell apoptosis-related protein Bax was decreased, and the expression of Bcl-2 was increased, the differences were highly statistically significant (P ＜ 0.01). Conclusion Fucoidan may protect the PD cell models through anti-oxidation, reducing the expression of Caspase-3 and inhibiting cell apoptosis.

Key words： Fucoidan Parkinson′s disease MN9D cell Oxidation stress Cell apoptosis

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	LIANG Zhigang1 SUN Xuwen1 LIU Zhuli1 YANG Shaowan1 LUO Dingzhen2

Cite this article:

LIANG Zhigang1 SUN Xuwen1 LIU Zhuli1 YANG Shaowan1 LUO Dingzhen2. The protective effect of fucoidan on oxidation stress and apoptosis of MN9D cells damaged by MPP+[J]. 中国医药导报, 2019, 16(7): 20-24.

URL:

http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2019/V16/I7/20

[1] Thomas B，Beal MF. Parkinson′s disease [J]. Hum Mol Genet，2007，16（2）：R183-R194.
[2] Dudas B，Rose M，Cornelli U，et al. Neuroprotective Properties of Glycosaminoglycans：Potential Treatment for Neurodegenerative Disorders [J]. Neurodegener Dis，2008，5（3/4）：200-205.
[3] Mariana B，Patrícia V，Andrade PB. Bioactive Compounds from Macroalgae in the New Millennium：Implications for Neurodegenerative Diseases [J]. Mar Drugs，2014，2（9）：4934-4972.
[4] Riederer P，Laux G. MAO-inhibitors in Parkinson′s Disease [J]. Exp Neurobiol，2011，20（1）：1-17.
[5] Kumar S，Okello EJ，Harris JR. Experimental inhibition of fibrillogenesis and neurotoxicity by amyloid-beta（Aβ）and other disease-related peptides/proteins by plant extracts and herbal compounds [J]. Subcell Biochem，2012，65：295-326.
[6] Von Stockum S，Nardin A，Schrepfer E，et al. Mitochondrial dynamics and mitophagy in Parkinson′s disease：A fly point of view [J]. Neurobio Dis，2016，90：58-67.
[7] Kim GH，Kim JE，Rhie SJ，et al. The Role of Oxidative Stress in Neurodegenerative Diseases [J]. Exp Neurobiol，2015，24（4）：325-340.
[8] Aldakheel A，Kalia LV，Lang AE. Pathogenesis-Targeted，Disease-Modifying Therapies in Parkinson Disease [J]. Neurotherapeutics，2014，11（1）：6-23.
[9] Soo PH，Jin HH，Gi-Young K，et al. Induction of Apoptosis by Fucoidan in Human Leukemia U937 Cells through Activation of p38 MAPK and Modulation of Bcl-2 Family [J]. Mar Drugs，2013，11（7）：2347-2364.
[10] Lehriboufala S，Ouidja MO，Hénault E，et al. New Roles of Glycosaminoglycans in α-Synuclein Aggregation in a Cellular Model of Parkinson Disease [J]. PLoS One，2015， 10（1）：e0116641.
[11] Lei T，Li H，Fang Z，et al. Polysaccharides from Angelica sinensis alleviate neuronal cell injury caused by oxidative stress [J]. Neural Regen Res，2014，9（3）：260-267.
[12] Lee DH，Kim CS，Lee YJ. Astaxanthin protects against MPTP/MPP+-induced mitochondrial dysfunction and ROS production in vivo and in vitr [J]. Food Chem Toxicol，201， 49（1）：271-280.
[13] Lu XL，Lin YH，Wu Q，et al. Paeonolum protects against MPP+ -induced neurotoxicity in zebrafish and PC12 cells [J]. BMC Complement Altern Med，2015，15：137.
[14] 梁志刚，孙旭文，李敏，等.褐藻多糖硫酸酯对1-甲基4-苯基吡啶离子损伤的MN9D细胞内氧化应激及组织蛋白酶D-单克隆凋亡相关蛋白的作用[J].临床神经病学杂志，2017，30（4）：285-289.
[15] Dias V，Junn E，Mouradian MM. The role of oxidative stress in Parkinson′s disease [J]. J Parkinsons Dis，2013， 3（4）：461-491.
[16] Zawada WM，Banninger GP，Thornton J，et al. Generation of reactive oxygen species in 1-methyl-4-phenylpyridinium（MPP+）treated dopaminergic neurons occurs as an NADPH oxidase-dependent two-wave cascade [J]. J Neuroinflammation，2011，8（1）：1-13.
[17] Rodríguezserrano M，Bárány I，Prem D，et al. NO，ROS，and cell death associated with caspase-like activity increase in stress-induced microspore embryogenesis of barley [J]. J Exp Bot，2012，63（5）：2007-2024.
[18] Zorov DB，Juhaszova M，Sollott SJ. Mitochondrial reactive oxygen species（ROS）and ROS-induced ROS releas [J]. Physiol Rev，2014，94（3）：909-950.
[19] Xiao DL，Zhang L. Upregulation of Bax and Bcl-2 following prenatal cocaine exposure induces apoptosis in fetal rat brain [J]. Int J Med Sci，2008，5（6）：295-302.
[20] Venderova K，Park DS. Programmed Cell Death in Parkinson′s Disease [J]. Cold Spring Harb Perspect Med，2011， 2（8）：591-605.
[21] Yan MH，Wang X，Zhu X. Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease [J]. Free Radic Biol Med，2013，62（9）：90-101.