title: Wnt3a protects SH-SY5Y cells against 6-hydroxydopamine toxicity by restoration of mitochondria function.
abstract: BACKGROUND
  Wnt/β-catenin signal has been reported to exert cytoprotective effects in cellular models of several diseases, including Parkinson's disease (PD). This study aimed to investigate the neuroprotective effects of actived Wnt/β-catenin signal by Wnt3a on SH-SY5Y cells treated with 6-hydroxydopamine (6-OHDA).
  
  
  METHODS
  Wnt3a-conditioned medium (Wnt3a-CM) was used to intervene dopaminegic SH-SY5Y cells treated with 6-OHDA. Cell toxicity was determined by cell viability and lactate dehydrogenase leakage (LDH) assay. The mitochondria function was measured by the mitochondrial membrane potential, while oxidative stress was monitored with intracellular reactive oxygen species (ROS). Western blot analysis was used to detect the expression of GSK3β, β-catenin as well as Akt.
  
  
  RESULTS
  Our results showed that 100 μM 6-OHDA treated for 24 h significantly decreased cell viability and mitochondrial transmembrane potential, reduced the level of β-catenin and p-Akt, increased LDH leakage, ROS production and the ratio of p-GSK3β (Tyr216) to p-GSK3β (Ser9). However, Wnt3a-conditioned medium reversing SH-SY5Y cells against 6-OHDA-induced neurotoxicity by reversing these changes.
  
  
  CONCLUSIONS
  Activating of Wnt/β-catenin pathway by Wnt3a-CM attenuated 6-OHDA-induced neurotoxicity significantly, which related to the inhibition of oxidative stress and maintenance of normal mitochondrial function.
authors.affiliation: Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630 China ; Department of Neurology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080 China.
authors.forename: Lei
authors.initials: L
authors.lastname: Wei
authors.affiliation: Department of pathology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080 China.
authors.forename: Li
authors.initials: L
authors.lastname: Ding
authors.affiliation: Department of Neurology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080 China.
authors.forename: Ming-Shu
authors.initials: MS
authors.lastname: Mo
authors.affiliation: Department of Neurology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080 China.
authors.forename: Ming
authors.initials: M
authors.lastname: Lei
authors.affiliation: Department of Neurology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080 China.
authors.forename: Limin
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Division of Clinical Laboratory, Zhongshan Hospital of Sun Yat-sen University, Zhongshan, 528403 China.
authors.forename: Kang
authors.initials: K
authors.lastname: Chen
authors.affiliation: Department of Neurology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080 China ; Department of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120 China.
authors.forename: Pingyi
authors.initials: P
authors.lastname: Xu
keywords: 6-OHDA; Mitochondria function; Parkinson’s disease; Wnt3a