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

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摘要目的探讨β-蜕皮甾酮通过激活PI3K/Akt通路对MPTP诱导的帕金森病（PD）小鼠体内神经保护作用。方法将42只小鼠采用随机数字表法分为正常组（A组），模型组（B组），司来吉兰组（C组），β-蜕皮甾酮高（D组）、中（E组）、低剂量组（F组），每组7只。观察行为学变化，Western blot检测脑内TH、PI3K和P-PI3K、Akt和P-Akt、BAX及BCL-2蛋白表达，RT-qPCR检测小鼠脑内BAX、BCL-2 mRNA表达。结果 B组小鼠爬杆时间长于A组，C、D、E组小鼠爬杆时间短于B组，差异有统计学意义（P＜0.05）。B组小鼠悬挂评分高于A组，C、D、E组小鼠悬挂评分低于B组，差异有统计学意义（P＜0.05）。B组P-PI3K/PI3K及P-PAkt/Akt比值低于A组，C、D、E组P-PI3K/PI3K及P-PAkt/Akt比值高于B组，差异有统计学意义（P＜0.05）。B组抑凋亡蛋白BCL-2表达低于A组，促凋亡蛋白BAX表达高于A组，差异有高度统计学意义（P＜0.01）；C、D、E组BCL-2蛋白表达高于B组，BAX蛋白表达低于B组，差异有统计学意义（P＜0.05）。B组BCL-2 mRNA表达量低于A组，C、D、E组BCL-2 mRNA表达量高于B组，差异有统计学意义（P＜0.05）。B组BAX mRNA表达量高于A组，C、D、E组BAX mRNA表达量低于B组，差异有统计学意义（P＜0.05）。结论 β-蜕皮甾酮以剂量依赖式激活PI3K/Akt通路保护MPTP诱导的PD小鼠的多巴胺能神经元，继而减弱细胞凋亡。

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	渠丽丽张英博董海影刘得水陈培培张晓杰

关键词 ：帕金森病；&beta, -蜕皮甾酮；PI3K/Akt通路；凋亡

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

基金资助:国家自然科学基金面上项目（81973597）。

通讯作者: 张晓杰（1965-），女，教授，博士生导师，主要从事神经退行性疾病的分子生物学研究。

作者简介: 渠丽丽（1996-），女，齐齐哈尔医学院病理学院2020级在读硕士研究生，主要从事神经退行性疾病的生物学研究。

引用本文:

渠丽丽张英博董海影刘得水陈培培张晓杰. β-蜕皮甾酮对MPTP诱导的帕金森病的体内保护研究[J]. 中国医药导报, 2022, 19(35): 4-7,16.
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. 中国医药导报, 2022, 19(35): 4-7,16.

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