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05), and this was significantly alleviated by 100?mg/kg KRG administration (p?Venetoclax cell line and p?Ibrutinib research buy in studies relating to the action of KRG in PD. Our study demonstrated that KRG can improve the behavioral impairment, protect dopaminergic neurons from MPTP-induced neuronal death, and suppress the MPTP-induced overexpression of Cdk5 and cleavage of p35 to p25 in the SN and the ST. To evaluate the effect of KRG on MPTP-induced behavioral impairment, the pole test was performed because it is a precise method that can perceive nigrostriatal dysfunction [19]. In addition, we confirmed dopaminergic neuronal death in SN and ST because MPTP induces persistent symptoms of PD by destroying dopaminergic neurons in the nigrostriatal system. We found that KRG administration dose-dependently alleviated MMP23B the behavioral impairment and suppressed dopaminergic neuronal death in the SN and ST, which suggests that KRG can alleviate MPTP-induced behavioral impairment by suppressing dopaminergic neuronal death in the nigrostriatal system. Although the mechanism by which Cdk5 mediates neuronal cell death in PD is not fully understood, it has been known that hyperactivation of Cdk5 plays an important role in pathogenesis of PD. Cdk5 is phosphorylated by p35 in normal conditions, which support neuronal survival [20]. However, MPTP injection enhances p25 levels by degradation of p35, which induces Cdk5 hyperactivity [21].