鸢尾苷元调控miR-103a-3p/SHC3通路对帕金森病模型细胞损伤的影响

李茜; 付子娟; 孙鹏; 曹亦宾

doi:10.16016/j.1000-5404.202106021

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鸢尾苷元调控miR-103a-3p/SHC3通路对帕金森病模型细胞损伤的影响

神经科学 | 更新时间：2026-01-09

- 鸢尾苷元调控miR-103a-3p/SHC3通路对帕金森病模型细胞损伤的影响
- Tectorigenin protects cell damage in Parkinson's disease model by regulating miR-103a-3p/SHC3 pathway
- 第三军医大学学报 2021年43卷第24期页码：2625-2632
- 作者机构：
  
  063000 河北唐山，唐山市工人医院神经内科
- 作者简介：
  
  [ 曹亦宾，E-mail:yibincao2019@163.com CAO Yibin, E-mail:yibincao2019@163.com
- 基金信息：
- DOI：10.16016/j.1000-5404.202106021
  中图分类号： R282.71;R285.5;R742.5
- 收稿：2021-06-03，
  
  修回：2021-08-19，
  
  纸质出版：2021-12-30
- 稿件说明：
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李茜, 付子娟, 孙鹏, 等. 鸢尾苷元调控miR-103a-3p/SHC3通路对帕金森病模型细胞损伤的影响[J]. 第三军医大学学报, 2021,43(24):2625-2632.

Qian LI, Zijuan FU, Peng SUN, et al. Tectorigenin protects cell damage in Parkinson's disease model by regulating miR-103a-3p/SHC3 pathway[J]. Journal of Third Military Medical University, 2021, 43(24): 2625-2632.
李茜, 付子娟, 孙鹏, 等. 鸢尾苷元调控miR-103a-3p/SHC3通路对帕金森病模型细胞损伤的影响[J]. 第三军医大学学报, 2021,43(24):2625-2632. DOI： 10.16016/j.1000-5404.202106021.

Qian LI, Zijuan FU, Peng SUN, et al. Tectorigenin protects cell damage in Parkinson's disease model by regulating miR-103a-3p/SHC3 pathway[J]. Journal of Third Military Medical University, 2021, 43(24): 2625-2632. DOI： 10.16016/j.1000-5404.202106021.

摘要

目的

探讨鸢尾苷元对帕金森病(Parkinson’s disease，PD)模型细胞损伤的影响，分析其是否与调控miR-103a-3p/含有Src同源结构域2的衔接蛋白3(SHC adaptor protein 3，SHC3)通路有关。

方法

用250 mmol/L的1-甲基-4-苯基吡啶离子(MPP

)诱导PC12建立PD细胞模型。PC12细胞分为对照组、PD组、PD+鸢尾苷元50 μmol/L组、PD+鸢尾苷元100 μmol/L组、PD+鸢尾苷元200 μmol/L组、PD+anti-miR-NC组、PD+miR-103a-3p Inhibitor组、PD+鸢尾苷元+miR-103a-3p mimic组。CCK-8法检测各组细胞活力，流式细胞术分析各组细胞凋亡率，试剂盒检测各组细胞超氧化物歧化酶(superoxide dismutase

SOD)活性、丙二醛(malondialdehyde

MDA)水平以及乳酸脱氢酶(lactate dehydrogenase

LDH)释放量，RT-qPCR检测miR-103a-3p表达，Werstern blot检测SHC3蛋白水平。双荧光素酶报告实验分析miR-103a-3p和SHC3靶向关系。

结果

与对照组比较，PD组PC12细胞活力、SOD活性、SHC3蛋白表达显著降低(

0.05)，凋亡率、MDA水平、LDH释放量、miR-103a-3p表达显著升高(

0.05)。与PD组比较，PD+鸢尾苷元50 μmol/L组、PD+鸢尾苷元100 μmol/L组、PD+鸢尾苷元200 μmol/L组PC12细胞活力、SOD活性、SHC3蛋白表达显著升高(

0.05)，凋亡率、MDA水平、LDH释放量、miR-103a-3p表达显著降低(

0.05)。与PD+anti-miR-NC组比较，PD+miR-103a-3p Inhibitor组PC12细胞活力、SOD活性、SHC3蛋白表达显著升高(

0.05)，凋亡率、MDA水平、LDH释放量显著降低(

0.05)。与PD+鸢尾苷元组比较，PD+鸢尾苷元+miR-103a-3p mimic组PC12细胞活力、SOD活性、SHC3蛋白表达显著降低(

0.05)，凋亡率、MDA水平、LDH释放量显著升高(

0.05)。miR-103a-3p与SHC3直接结合。

结论

鸢尾苷元可保护PD模型细胞凋亡和氧化损伤，其机制与抑制miR-103a-3p/SHC3通路有关。

Abstract

Objective

To investigate the effect of tectorigenin on cell model of Parkinson's disease (PD)

so as to further analyze whether its mechanism is related to the regulation of miR-103a-3p/SHC adaptor protein 3 (SHC3) pathway.

Methods

PC12 cells were treated with 250 mmol/L 1-methyl-4-phenylpyridine ion (MPP

) to establish a PD cell model. Then

the cells were divided into control group and experimental groups as follows: PD group

PD+50 μmol/L tectorigenin

PD+100 μmol/L tectorigenin

PD+200 μmol/L tectorigenin

PD+anti-miR-NC

PD+miR-103a-3p inhibitor

and PD+tectorigenin+miR-103a-3p mimic. Cell viability and apoptotic rate of each group were evaluated using CCK-8 assay and flow cytometry respectively. The activity of superoxide dismutase (SOD)

content of malondialdehyde (MDA) and release of lactate dehydrogenase (LDH) of cells in each group were subsequently detected. Moreover

RT-qPCR and Western blotting were performed to determine the mRNA expression of miR-103a-3p and protein level of SHC3

respectively

and dual luciferase reporting assay was adopted to analyze the targeting relationship between miR-103a-3p and SHC3.

Results

As compared with the control group

the viability

SOD activity

and SHC3 expression of cells were notably reduced (

0.05)

while the apoptotic rate

MDA content

LDH release

and miR-103a-3p expression were significantly increased (

0.05) in the PD group. When compared with the PD group

the viability

SOD activity

and SHC3 expression of cells in the PD+tectorigenin (50

100 and 200 μmol/L) groups were all notably improved (

0.05)

while the apoptotic rate

MDA content

LDH release and miR-103a-3p level were greatly declined (

0.05). In addition

the cell viability

SOD activity and SHC3 level were higher

whereas the apoptotic rate

MDA content and LDH release were lower in the PD+miR-103a-3p inhibitor group than in the PD+anti-miR-NC group (

0.05). Finally

the ce

ll viability

SOD activity and SHC3 expression in the PD+tectorigenin+miR-103a-3p mimic group were notably decreased (

0.05)

while the apoptotic rate

MDA content

and LDH release were increased (

0.05)

as compared with the PD+tectorigenin groups. Dual luciferase reporting assay showed that SHC3 was a direct target of miR-103a-3p.

Conclusion

Tectorigenin protects PD model cells against apoptosis and oxidative damage

which may be related to the inhibition of miR-103a-3p/SHC3 pathway.

关键词

Keywords

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