Abstract
The neuroprotective effects of (±)-catechin against toxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were investigated in mice. MPTP caused the death of dopaminergic neurons in the substantia nigra and decreased the level of striatal dopamine. Additionally, MPTP increased the level of phospho-c-Jun, a known substrate of c-Jun N-terminal kinase (JNK) and caused a rapid activation of GSK-3β, evidenced by the decrease in the level of phospho-Ser9 of GSK-3β. However, pretreatment with (±)-catechin was found to protect dopaminergic neurons in the substantia nigra against MPTP toxicity, and restore the depletion of striatal dopamine in mice. (±)-Catechin attenuated the phosphorylation of c-Jun and recovered the phosphorylation of GSK-3β (Ser9). These results suggested that the suppression of JNK and GSK-3β signaling cascades might contribute to the neuroprotective effect of (±)-catechin against toxicity of MPTP.
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