Catalpol Exerts Neuroprotective Effect on 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP)-Induced Mouse Model of Parkinson’s Disease and the Underlying Mechanisms

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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“…Autopsy studies, as well as animal models of MPTP and 6-OHDA neurodegeneration, show that JNK plays an important role in the pathogenesis of the disease ( Iqbal et al, 2015 ). In a study evaluating the effect of catalpol on MPTP treated mice to establish PD model, the results showed that catalpol affected MKK4/JNK/cJun signaling pathway, reduced the loss of dopamine neurons, increased TH expression and delayed MPTP induced oxidative stress ( Li and Zhao, 2021 ).…”

“…In a study evaluating the effect of catalpol on MPTP treated mice to establish PD model, the results showed that catalpol affected MKK4/JNK/cJun signaling pathway, reduced the loss of dopamine neurons, increased TH expression and delayed MPTP induced oxidative stress (Li and Zhao, 2021).…”