Abstract
Our current study aimed to assess the preventive and therapeutic impacts of catalpol on Parkinson’s disease (PD) and its possible mechanism. In this study, mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were employed to establish a PD model and then treated with catalpol followed by analysis of behavioral science by open field test, pole-climbing assay and rotarod performance test, ROS and SOD activity and expression of TH, DAT, VEGF and GAP43 by western blot or immunofluorescence. The results disclosed that catalpol can ameliorate the MPTP-triggered loss of dopamine (DA)-producing neurons, while it was able to enhance the expression of tyrosine hydroxylase (TH), accompanied by the activation of astrocytes and microglia. Catalpol treatment significantly retarded the oxidative stress induced by MPTP, along with elevated levels of VEGF and growth-associated protein 4 (GAP43). Additionally, catalpol treatment activated the MKK4/JNK/c-Jun signal pathway in PD mouse model, accompanied by reduced secretion of pro-inflammatory factors. Catalpol executed the anti-apoptotic and anti-oxidant impacts on MPTP-induced Parkinson’s model, suggesting that it might be a novel approach for treating PD in the future.
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