第一季
MFN1型
MFN2型
线粒体融合
线粒体
免疫印迹
细胞生物学
DNM1L型
程序性细胞死亡
线粒体分裂
化学
生物
分子生物学
细胞凋亡
生物化学
线粒体DNA
基因
作者
Cong Gai,Wan-Di Feng,Tian-Yao Qiang,Haojie Ma,Yuan Chai,Shujing Zhang,Zhenyu Guo,Jinghong Hu,Hong‐Mei Sun
标识
DOI:10.3389/fphar.2019.00372
摘要
To investigate the effect of Da-Bu-Yin-Wan and Qian-Zheng-San (DBYW & 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 & QZS. CCK-8 method was used to detect the survival rate of cells in each group. Mitochondria was labeled by mitoTracker® Red CMXRos (MTR) probe and observed by laser scanning confocal microscope, and ImageJ software was used to process images and measure mitochondrial form factors; TMRM 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. After MPP+ modeling, the cell survival rate, form factor (F-factor) and mitochondrial activity were decreased significantly. ΔΨm and ATP levels were decreased significantly. The expression levels of Parkin protein, Mfn1, Mfn2 and OPA1 were decreased significantly. However, MPP+ treatment would dramatically increase the expression of Drp1 and Fis1. Compared with the model group, after treatment with DBYW & QZS, the cell survival rate, mitochondrial form factors and activity, ΔΨm were increased significantly; while the increase of ATP levels was not significantly. Additionally, DBYW & QZS significantly increased expression of Parkin protein and Mfn1, Mfn2 and OPA1 and a trend towards reduced expression of Drp1 and Fis1. DBYW & QZS has a certain protective effect on the injury of PD cells model induced by MPP+. The mechanism is associated with regulation the homeostasis between mitochondrial fission and fusion.
科研通智能强力驱动
Strongly Powered by AbleSci AI