β-蜕皮甾酮对MPTP诱导的帕金森病的体内保护研究

doi:10.20047/j.issn1673-7210.2022.35.01

Abstract
Figure/Table
References (26)
Related Citation (1)

Download: PDF (1768 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective To investigate the in vivo neuroprotective effect of β-ecdysterone on MPTP (MPTP)-induced Parkinson’s disease (PD) mice through activation of the PI3K/Akt pathway. Methods Forty-two mice were divided into normal group (group A), model group (group B), sregiline group (group C), β-ecdysterone high group (group D), medium group (group E), and low dose (group F) group by random number table method, with seven mice in each group. Behavioral changes were observed, TH, PI3K, and P-PI3K, Akt and P-Akt, BAX, and BCL-2 protein expression in the brain were detected by Western blot, and BAX and BCL-2 mRNA expression in the brain of mice were detected by RT-qPCR. Results Mice in group B took longer to climb the pole than those in group A, while mice in groups C, D, and E took shorter time to climb the pole than those in group B, and the differences were statistically significant (P＜0.05). The suspension scores of mice in group B were higher than those in group A, while the suspension scores of mice in groups C, D, and E were lower than those in group B, and the differences were statistically significant (P＜0.05). The P-PI3K/PI3K and P-PAkt/Akt ratios in group B were lower than those in group A, while the P-PI3K/PI3K and P-PAkt/Akt ratios in groups C, D, and E were higher than those in group B, and the differences were statistically significant (P＜0.05). The expression of apoptosis-inhibiting protein BCL-2 in group B was lower than that in group A, while the expression of pro-apoptosis protein BAX was higher than that in group A, and the differences were highly statistically significant (P＜0.01); the expression of BCL-2 protein in groups C, D, and E were higher than that in group B, while the expression of BAX protein were lower than that in group B, and the differences were statistically significant (P＜0.05). The expression of BCL-2 mRNA in group B was lower than that in group A, while the expression of BCL-2 mRNA in groups C, D, and E were higher than that in group B, and the differences were statistically significant (P＜0.05). The expression of BAX mRNA in group B was higher than that in group A, while the expression of BAX mRNA in groups C, D, and E were lower than that in group B, and the differences were statistically significant (P＜0.05). Conclusion β-Ecdysterone protects dopaminergic neurons in MPTP-induced PD mice with dose-dependent activation of the PI3K/Akt pathway, which subsequently attenuates apoptosis.

Key words： Parkinson’s disease β-ecdysterone PI3K/Akt pathway Apoptosis

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	QU Lili ZHANG Yingbo DONG Haiying LIU Deshui CHEN Peipei ZHANG Xiaojie

Cite this article:

QU Lili ZHANG Yingbo DONG Haiying LIU Deshui CHEN Peipei ZHANG Xiaojie. In vivo protection study of β-ecdysterone against MPTP-induced Parkinson’s disease[J]. 中国医药导报, 2022, 19(35): 4-7,16.

URL:

https://www.yiyaodaobao.com.cn/EN/10.20047/j.issn1673-7210.2022.35.01 OR https://www.yiyaodaobao.com.cn/EN/Y2022/V19/I35/4

[1] Schapira AHV，Chaudhuri KR，Jenner P. Non-motor features of Parkinson disease [J]. Nat Rev Neurosci，2017，18（7）：435-450.
[2] Opara J，Ma?覥ecki A，Ma?覥ecka E，et al. Motor assessment in Parkinson’s disease [J]. AAEM，2017，24（3）：411-415.
[3] 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.
[4] 林杰，陈涛，苏佳丽，等.线粒体功能障碍在帕金森病发病机制研究中的新进展[J].中国医师杂志，2021，23（8）：1269-1274.
[5] 刘慧，张自弘，鲍秀琦，等.线粒体动力学和线粒体自噬的分子机制及其在神经退行性疾病中的作用[J].中国药学杂志，2020，55（5）：337-341.
[6] 苏燕，周亚莉，田琳琳，等.中药活性成分防治帕金森病的研究进展[J].神经解剖学杂志，2020，36（1）：111-115.
[7] 刘国安，杨庆明，侯国鹏，等.牛膝总皂甙的体外抗氧化性研究[J].天然产物研究与开发，2006（6）：975-977.
[8] 李俊丽，韩兴发，刘铁秋，等.川牛膝多糖对衰老小鼠模型的体内抗氧化作用[J].中国抗生素杂志，2014，39（7）：553-559.
[9] 邹德平，许志忠，曹灵，等.蜕皮甾酮对实验性糖尿病大鼠肾组织氧化应激的影响[J].中国中西医结合肾杂志，2010，11（1）：28-30，97.
[10] Hu J，Luo CX，Chu WH，et al. 20-Hydroxyecdysone protects against oxidative stress-induced neuronal injury by scavenging free radicals and modulating NF-κB and JNK pathways [J]. PLoS One，2012，7（12）：e50764.
[11] 罗菡，罗春霞，张映琦，等.蜕皮甾酮对大鼠局灶性脑缺血脂质过氧化损伤的影响[J].中国药业，2009，18（15）：12-14.
[12] Cai YJ，Dai JQ，Fang JG，et al. Antioxidative and free radical scavenging effects of ecdysteroids from Serratula strangul- ata [J]. Can J Physiol Pharmacol，2002，80（12）：1187-1194.
[13] 谢静文，苏天德，魏雨亭，等.抗氧化药物在心肌缺血再灌注损伤中的研究进展[J].药学学报，2021，56（7）：1845-1855.
[14] Komnig D，Dagli TC，Habib P，et al. Fingolimod （FTY720） is not protective in the subacute MPTP mouse model of Parkinson’s disease and does not lead to a sustainable increase of brain-derived neurotrophic factor [J]. J Neurochem，2018，147（5）：678-691.
[15] Reich SG，Savitt JM. Parkinson’s Disease [J]. Med Clin North Am，2019，103（2）：337-350.
[16] Wen Z£¬Zhang J£¬Tang P£¬et al. Overexpression of miR-185 inhibits autophagy and apoptosis of dopaminergic neurons by regulating the AMPK/mTOR signaling pathway in Parkinson¡¯s disease [J]. Mol Med Rep£¬2018£¬17£¨1£©£º131- 137.
[17] Yoosefian M£¬Rahmanifar E£¬Etminan N. Nanocarrier for levodopa Parkinson therapeutic drug; comprehensive benserazide analysis [J]. Artif Cells£¬2018£¬46£¨sup1£©£º434- 446.
[18] Elkouzi A£¬Vedam-Mai V£¬Eisinger RS£¬et al. Emerging therapies in Parkinson disease-repurposed drugs and new approaches [J]. Nat Rev Neurol£¬2019£¬15£¨4£©£º204-223.
[19] Pan Z£¬Niu Y£¬Liang Y£¬et al. ¦Â-Ecdysterone Protects SH-SY5Y Cells Against 6-Hydroxydopamine-Induced Apoptosis via Mitochondria-Dependent Mechanism£ºInvolvement of p38£¨MAPK£©-p53 Signaling Pathway [J]. Neurotox Res£¬2016£¬ 30£¨3£©£º453-466.
[20] Zhang QS£¬Heng Y£¬Mou Z£¬et al. Reassessment of subacute MPTP-treated mice as animal model of Parkinson¡¯s disease [J]. Acta Pharmacol Sin£¬2017£¬38£¨10£©£º1317-1328.
[21] Nakashima A£¬Ota A£¬Kaneko YS£¬et al. A possible pathophysiological role of tyrosine hydroxylase in Parkinson¡¯s disease suggested by postmortem brain biochemistry£ºa contribution for the special 70th birthday symposium in honor of Prof. Peter Riederer [J]. J Neural Transm£¬2013£¬ 120£¨1£©£º49-54.
[22] Wang T£¬Li C£¬Han B£¬et al. Neuroprotective effects of Danshensu on rotenone-induced Parkinson¡¯s disease models in vitro and in vivo [J]. BMC Complement Med Ther£¬2020£¬20£¨1£©£º20.
[23] Zou Y£¬Wang R£¬Guo H£¬et al. Phytoestrogen ¦Â-Ecdysterone Protects PC12 Cells Against MPP+-Induced Neurotoxicity In Vitro£ºInvolvement of PI3K-Nrf2-Regulated Pathway [J]. Toxicol Sci£¬2015£¬147£¨1£©£º28-38.
[24] Kume T. Therapeutic Potential of the Activators of the Nuclear Factor Erythroid 2-Related Factor 2-Antioxidant Response Element Pathway in Brain Disorders [J]. Biol Pharm Bull£¬2017£¬40£¨5£©£º553-556.
[25] Whelan RS£¬Kaplinskiy V£¬Kitsis RN. Cell death in the pathogenesis of heart disease£ºmechanisms and significance [J]. Annu Rev Physiol£¬2010£¬72£º19-44.
[26] Hu M£¬Li F£¬Wang W. Vitexin protects dopaminergic neurons in MPTP-induced Parkinson¡¯s disease through PI3K/ Akt signaling pathway [J]. Drug Des Devel Ther£¬2018£¬12£º565-573.