Propofol protects against the neurotoxicity of 1-methyl-4-phenylpyridinium.

Parkinson's disease (PD) is a progressive and degenerative disorder of the central nervous system, characterized by the loss of dopaminergic neurons and muscular rigidity. Treatment with propofol (2,6-diisopropylphenol) has been observed to attenuate oxidative stress injury via inhibition of programmed cell death. Results from the present study indicate that propofol treatment attenuates 1-methyl-4-phenylpyridinium (MPP⁺)-induced oxidative stress, which was demonstrated by increased levels of reactive oxygen species, 4-hydroxy-2-nonenal and protein carbonyls. Furthermore, it was demonstrated that propofol may ameliorate MPP⁺-induced mitochondrial dysfunction by increasing the level of ATP and the mitochondrial membrane potential. MTT and lactate dehydrogenase assays indicated that propofol treatment reduces cell vulnerability to MPP⁺-induced insult. Propofol was also observed to prevent apoptotic signals by reducing the ratio of Bcl-2-associated X protein to B-cell lymphoma 2, reducing the expression level of cleaved caspase-3 and attenuating cytochrome c release. Thus, propofol may present as a novel therapeutic strategy for the treatment of PD. [ABSTRACT FROM AUTHOR]