Propofol protects against the neurotoxicity of 1‑methyl‑4‑phenylpyridinium

Wang,Shoushi; Song,Tingting; Leng,Cuibo; Lan,Ketao; Ning,Jishun; Chu,Haichen

doi:10.3892/mmr.2015.4570

Propofol protects against the neurotoxicity of 1‑methyl‑4‑phenylpyridinium

Authors:
- Shoushi Wang
- Tingting Song
- Cuibo Leng
- Ketao Lan
- Jishun Ning
- Haichen Chu
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Affiliations: Department of Anesthesiology, Qingdao Central Hospital, Qingdao, Shandong 266042, P.R. China, Department of Oncology, Qingdao Central Hospital, Qingdao, Shandong 266042, P.R. China, Department of Cardiology, Qingdao Central Hospital, Qingdao, Shandong 266042, P.R. China, Department of Anesthesiology, Affiliated Hospital of Qingdao University Medical College, Qingdao, Shandong 266003, P.R. China
Published online on: November 16, 2015 https://doi.org/10.3892/mmr.2015.4570
Pages: 309-314

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Abstract

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.

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