Repetitive transcranial magnetic stimulation for treatment of lactacystin-induced Parkinsonian rat model
Metrics: PDF 538 views | HTML 966 views | ?
Maowen Ba1,*, Guozhao Ma2,*, Chao Ren1 , Xuwen Sun1 and Min Kong3
1Department of Neurology, Yantai Yuhuangding Hospital Affiliated to Qingdao Medical University, Yantai 264000, Shandong, PR China
2Department of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, 250014, Shandong, PR China
3Department of Neurology, Yantaishan Hospital, Yantai City, Shandong 264000, PR China
*These authors contributed equally to this work
Min Kong, email: email@example.com
Xuwen Sun, email: firstname.lastname@example.org
Keywords: rTMS, Parkinson's disease, ubiquitin-proteasome system, dopamine, apoptosis
Received: September 26, 2016 Accepted: April 11, 2017 Published: April 20, 2017
The dysfunction of ubiquitin-proteasome system is an important pathogenesis in the neurodegenerative process of Parkinson's disease. Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive and potential method in treating Parkinson's disease. To investigate whether rTMS has neuroprotective effects in parkinsonian rat model induced by ubiquitin-proteasome system impairment, we gave rTMS daily for 4 weeks to proteasome inhibitor, lactacystin-induced parkinsonian rat model. Rotational behavior test demonstrated that rTMS obviously reduced apomorphine-induced turning number in parkinsonian rats. rTMS could significantly alleviate the loss of tyrosine hydroxylase-positive dopaminergic neurons in lactacystin-lesioned substantia nigra and prevent the loss of striatal dopamine levels. Furthermore, rTMS also reduced the levels of apoptotic protein (cleaved caspase-3) and inflammatory factors (cyclooxygenase-2 and tumor necrosis factor alpha) in lesioned substantia nigra. These results suggest that rTMS can protect nigral dopaminergic neurons against the ubiquitin-proteasome system impairment-induced degeneration by anti-apoptotic and anti-inflammatory molecular mechanism.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.