Protective effects of DL-3-n-butylphthalide in the lipopolysaccharide-induced mouse model of Parkinson's disease
Authors:
- 1 May 2017
- journal article
- Published by Spandidos Publications in Molecular Medicine Reports
- Vol. 16 (5) , 6184-6189
Abstract
DL‑3‑n‑butylphthalide (NBP) is extracted from rapeseed and exhibits multiple neuroprotective effects, exerted by inhibiting the inflammatory process, including reducing oxidative stress, improving mitochondrial function and reducing neuronal apoptosis. The present study aimed to investigate the neuroprotective effects of NBP in a lipopolysaccharide (LPS)‑induced mouse model of Parkinson's disease (PD). The behavior of mice was assessed using the rotarod test and open‑field test, the amount of tyrosine hydroxylase in the substantia nigra pars compacta was evaluated by immunohistochemistry, and the levels of phosphorylated c‑Jun N‑terminal kinase (JNK), mitogen‑activated protein kinase 14 (p38) and extracellular signal‑regulated kinase 1 were determined by western blotting. It was demonstrated that the LPS‑induced behavioral deficits were significantly improved. LPS‑induced dopaminergic neurodegeneration was relieved following treatment with NBP, as determined from tyrosine hydroxylase‑positive cells. Phosphorylation of JNK and p38 was significantly inhibited following treatment with NBP. Therefore in the present study, a role for NBP has been established in the treatment of a PD murine model, laying the experimental basis for the treatment of PD with this agent.Keywords
This publication has 33 references indexed in Scilit:
- Quantitative assessment of gait and neurochemical correlation in a classical murine model of Parkinson’s diseaseBMC Neuroscience, 2012
- Oxidative Stress in Neurodegenerative Diseases and AgeingOxidative Medicine and Cellular Longevity, 2012
- The Role of p38 MAPK and Its Substrates in Neuronal Plasticity and Neurodegenerative DiseaseJournal of Signal Transduction, 2012
- Impaired mitochondrial biogenesis contributes to depletion of functional mitochondria in chronic MPP+ toxicity: dual roles for ERK1/2Cell Death & Disease, 2012
- Region-specific tauopathy and synucleinopathy in brain of the alpha-synuclein overexpressing mouse model of Parkinson's diseaseBMC Neuroscience, 2011
- Activation and Function of the MAPKs and Their Substrates, the MAPK-Activated Protein KinasesMicrobiology and Molecular Biology Reviews, 2011
- JNK Inhibition Protects Dopamine Neurons and Provides Behavioral Improvement in a Rat 6-Hydroxydopamine Model of Parkinson’s DiseaseACS Chemical Neuroscience, 2011
- dl-3-n-Butylphthalide prevents neuronal cell death after focal cerebral ischemia in mice via the JNK pathwayBrain Research, 2010
- The lipopolysaccharide Parkinson’s disease animal model: mechanistic studies and drug discoveryFundamental & Clinical Pharmacology, 2008
- Inflammation as a causative factor in the aetiology of Parkinson's diseaseBritish Journal of Pharmacology, 2007