Da-Bu-Yin-Wan and Qian-Zheng-San Ameliorate Mitochondrial Dynamics in the Parkinson’s Disease Cell Model Induced by MPP+

Abstract

To investigate the effect of Da-Bu-Yin-Wan and Qian-Zheng-San (DBYW and QZS) on mitochondrial mass in Parkinson’s disease (PD) cell model induced by 1-Methyl-4-phenylpyridinium Ion (MPP + ). The SH-SY5Y cell was selected and treated with MPP + . The PD model was intervened with DBYW and QZS. CCK-8 method was used to detect the survival rate of cells in each group. Mitochondria was labeled by mitoTracker ® Red CMXRos probe and observed by laser scanning confocal microscope, and ImageJ software was used to process images and measure mitochondrial form factors; Tetramethylrhodamine methyl ester was used to detect mitochondrial membrane potential (ΔΨm); Luciferase method was used to detect cellular ATP levels; Western-Blot technique was applied to detect the expression levels of Parkin protein, and the expression levels of Mfn1, Mfn2, OPA1, Drp1, and Fis1. We found that DBYW and QZS treatment significantly increased the cell survival rate, form factor (F-factor), mitochondrial activity and ΔΨm after MPP + treatment, while the increase of ATP levels was not significant. In addition, the results of western blot analysis showed that the MPP + induced increase in the expression of Drp1 and Fis1, as well as decrease in Parkin, Mfn1, Mfn2, and OPA1 were all partially revised by DBYW and QZS. In summary, our data strongly suggested that DBYW and QZS treatment can exert protective effects against PD related neuronal injury through regulation the homeostasis between mitochondrial fission and fusion.

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“…We found that BYQZF rescued MPP + -induced mitochondrial alterations, including ΔΨm and ATP levels in the negative treatment group, consistent with a previous study (Gai et al, 2019). However, BYQZF did not rescue mitochondrial dysfunction in MPP + -induced SH-SY5Y cells transfected with the parkin-knockdown plasmid.…”

Bu-Yin-Qian-Zheng Formula Ameliorates MPP+-Induced Mitochondrial Dysfunction in Parkinson’s Disease via Parkin

“…The protective effects of BYQZF on mitochondrial function have been confirmed in in vitro and in vivo studies (Zhang et al, 2013;Zhang et al, 2018;Gai et al, 2019); parkin was found to play an important role in this process. However, the mechanisms by which BYQZF ameliorates mitochondrial dysfunction via parkin are unclear.…”

“…Our previous studies showed that Da-Bu-Yin-Wan ameliorates MPTP-induced behavioral impairment, increases the expression of tyrosine hydroxylase in the substantia nigra, and prevents loss of substantia nigra dopaminergic neurons in a PD mouse model (Gong et al, 2014). Moreover, Da-Bu-Yin-Wan and/or Qian-Zheng-San significantly increase ATP levels and complex I activity in the midbrain tissue of PD model mice (Zhang et al, 2013), and BYQZF reduced mitochondrial damage and improved the mitochondrial morphological structure in a cellular model of PD (Zhang et al, 2018;Gai et al, 2019). These studies suggest that BYQZF had neuroprotective effects on mitochondrial function and may be applicable as a mitochondrion-targeted therapeutic drug for treating PD.…”

Effects of Acupuncture on Neurological Disease in Clinical- and Animal-Based Research

“…With the extensive use of acupuncture as an ASM therapy for PD, the mechanisms based on animal model of acupuncture treatment for PD were widely investigated. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1-methyl-4-phenylpyridinium (MPP+), 6-hydroxydopamine (6-OHDA) and rotenone are widely used as inducers in animal models of PD (Andrzejewski et al, 2019; Gai et al, 2019; He et al, 2019).…”