Neuroprotective effect of combined therapy with hyperbaric oxygen and madopar on 6-hydroxydopamine-induced Parkinson’s disease in rats

• Published in: Neuroscience letters 2015-07, Vol.600, p.220-225
• Main Authors: Pan, Xiaorong, Chen, Chunxia, Huang, Jianping, Wei, Haiming, Fan, Qiuping
• Format: Article
• Language: English
• Subjects: Animals; Apomorphine - pharmacology; Apoptosis; Benserazide - therapeutic use; Combined Modality Therapy; Drug Combinations; Glial Fibrillary Acidic Protein - metabolism; Glutathione Peroxidase - metabolism; HBO; Hyperbaric Oxygenation; Levodopa - therapeutic use; Lipid Peroxidation; Madopar; Male; Malondialdehyde - metabolism; Nerve Degeneration - etiology; Nerve Degeneration - metabolism; Nerve Degeneration - pathology; Nerve Degeneration - therapy; Neuroprotective Agents - therapeutic use; Oxidative Stress; Oxidopamine - therapeutic use; Parkinson Disease - etiology; Parkinson Disease - metabolism; Parkinson Disease - pathology; Parkinson Disease - therapy; Parkinson’s disease; Proto-Oncogene Proteins c-bcl-2 - metabolism; Rats, Wistar; Stereotyped Behavior; Substantia nigra; Substantia Nigra - metabolism; Substantia Nigra - pathology; Superoxide Dismutase - metabolism; Tyrosine 3-Monooxygenase - metabolism
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2015.06.030

[Display omitted] •The combination therapy attenuated apomorphine-induced turns in PD rats.•The combination therapy reduced oxidative stress and modulated the level of anti-apoptosis.•The combination inhibited neurodegeneration of PD rats. Parkinson’s disease (PD) is a common movement disorder in the elderly. In the present study, we examined whether the combination of hyperbaric oxygen (HBO) and madopar therapy provided a neuroprotective effect on dopaminergic neurons in the substantia nigra using a rat model of PD. Rotational assessments revealed that both HBO and combination therapy significantly attenuated apomorphine-induced turning in PD rats. Our results indicated that the combination therapy increased glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities and reduced the malondialdehyde (MDA) content in the SN. Furthermore, the combination therapy resulted in significant protection against the loss of neurons, and specifically tyrosine hydroxylase (TH)-positive neurons, in the SN and also alleviated the production of glial fibrillary acidic protein (GFAP). The levels of Bcl-2 were increased and Bax were decreased following the HBO or combination therapy. In brief, the neuroprotective effect of combined therapy with HBO and madopar against 6-OHDA-induced PD rats may rely on its ability to reduce oxidative stress and protect against Bax/Bcl-2-mediated apoptosis.