Artemisinin exerts a protective effect in the MPTP mouse model of Parkinson's disease by inhibiting microglial activation via the TLR4/Myd88/NF‐KB pathway

Abstract

AbstractAimsWe performed cell and animal experiments to explore the therapeutic effect of artemisinin on Parkinson's disease (PD) and the TLR4/Myd88 signaling pathway.MethodsC57 mice were randomly divided into the blank, 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐induced and artemisinin‐treated groups. Clinical symptoms, the number of dopaminergic (DAergic) neurons in the substantia nigra, and microglial cell activation were compared among the three groups. Subsequently, BV‐2 cell activation and TLR4/Myd88 pathway component expression were compared among the blank, MPP+‐treated, artemisinin‐treated, and TLR4 activator‐treated groups.ResultsBehavioral symptoms were improved, the number of DAergic neurons in the substantia nigra of the midbrain was increased, and microglial cell activation was decreased in artemisinin‐treated MPTP‐induced PD model mice compared with control‐treated MPTP‐induced PD model mice (p < 0.05). The cell experiments revealed that artemisinin treatment reduced MPP+‐induced BV‐2 cell activation and inhibited the TLR4/Myd88 signaling pathway. Moreover, the effect of artemisinin on the BV‐2 cell model was inhibited by the TLR4 activator LPS (p < 0.05).ConclusionArtemisinin may reduce damage to DAergic neurons in a PD mouse model by decreasing microglial activation through the TLR4‐mediated MyD88‐dependent signaling pathway. However, this finding cannot explain the relationship between microglia and DAergic neurons.