Mechanism of mitochondrial protection by the Buyin Qianzheng formula in a Parkin overexpression cell model
- Author:
Cheng CUICUI
1
;
Gao YUSHAN
;
Gai CONG
;
Feng WANDI
;
Ma HAOJIE
;
Feng JING
;
Guo ZHENYU
;
Zhang SHUJING
;
Wu JIE
;
Sun HONGMEI
Author Information
1. School of Traditional Chinese Medicine,Beijing University of Chinese Medicine,Beijing,102488,China
- Keywords:
Parkinson's disease;
Parkin overexpression;
Mitochondria;
Buyin Qianzheng formula;
Neumtoxin 1-methyl-4-phenylpyridinium ion;
SH-SY5Y;
Mitofusin 2;
Dynamic-related protein 1
- From:
Journal of Traditional Chinese Medical Sciences
2022;9(1):59-68
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To identify the molecular mechanisms of the effects of the Buyin Qianzheng formula (BYQZF)on the mitochondrial dynamics in a Parkin overexpression Parkinson's disease (PD) cell model.Methods:First,a stable Parkin overexpression cell model was constructed using plasmid transfection.Then,we examined the protective effect of BYQZF on the mitochondrial dysfunction of the Parkin overexpression PD cell model induced by neurotoxin 1-methyl-4-phenylpyridinium ion (MPP+).The mRNA expression level of Parkin was evaluated using real-time quantitative PCR.The cell survival rate was detected using the Cell Counting Kit-8 assay.We evaluated the cellular adenosine triphosphate (ATP)levels using luciferase assays.A laser scanning confocal microscope was used to observe the mito-chondrial morphology,activity,and mitochondrial membrane potential (ΔΨm).Western blot was con-ducted to evaluate the levels of the fusion proteins mitofusin1,mitofusin2,optic atrophy 1,dynamin-related protein 1,and mitochondrial fission protein 1.Results:Parkin overexpression attenuated MPP+-induced mitochondrial damage,increased mitochon-drial activity and AΨm.BYQZF increased the survival of MPP+-induced cells that overexpressed Parkin and upregulated the mitochondrial form factor and activity.It also inhibited a decrease in the ΔΨm and ATP levels.These findings suggested that BYQZF protected against MPP+-induced mitochondrial dysfunction and enhanced the protective effect of Parkin overexpression.Furthermore,the formula upregulated the expression of the fusion proteins mitofusin1,mitofusin2,and optic atrophy 1 (closely related to mitochondrial quality remodeling),and reduced the expression of the fission protein dynamic-related protein 1,as well as mitochondrial fission protein 1.Conclusion:The mechanism by which BYQZF increased the mitochondrial protective effect of Parkin gene overexpression in MPP+-induced cells may be related to improving mitochondrial function and regulating the balance of mitochondrial division and fusion proteins.
