DL­3­n­butylphthalide reduces microglial activation in lipopolysaccharide­induced Parkinson's disease model mice.

As microglial activation is a key factor in the pathogenesis of Parkinson's disease (PD), drugs that target this process may help to prevent or delay the development of PD. The present study investigated the effects of dl­3­n­butylphthalide (NBP) on microglia in a lipopolysaccharide (LPS)-induced PD mouse model. The mice were randomly divided into a blank control group, LPS control group and NBP + LPS treatment group. Mice in the treatment group were given an intragastric infusion of 120 mg/kg NBP daily for 30 days during the establishment of the PD mouse model. At 4 and 28 weeks post­treatment, the motor behaviours of the mice in each group were observed using the rotarod test and the open field test. In addition, immunohistochemical staining was performed to determine the levels of activated microglia, tumour necrosis factor­α and α­synuclein, and the number of tyrosine hydroxylase (TH)­positive cells in the substantia nigra. NBP significantly improved dyskinesia, reduced microglial activation, decreased nuclear α­synuclein deposition and increased the survival of TH­positive cells in the substantia nigra of LPS­induced PD model mice. These findings suggested that NBP may exert its therapeutic effect by reducing microglial activation in a mouse model of PD.