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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.

Protective effects of DL-3-n-butylphthalide in the lipopolysaccharide-induced mouse model of Parkinson's disease