Abstract
BackgroundMitochondrial dysfunction and oxidative stress are the main toxic events leading to dopaminergic neuronal death in Parkinson’s disease (PD) and identified as vital objective for therapeutic intercession. This study investigated the neuro-protective effects of the demethoxycurcumin (DMC), a derivative of curcumin against rotenone induced neurotoxicity.MethodsSH-SY5Y neuroblastoma cells are divided into four experimental groups: untreated cells, cells incubated with rotenone (100 nM), cells treated with DMC (50 nM) + rotenone (100 nM) and DMC alone treated. 24 h after treatment with rotenone and 28 h after treatment with DMC, cell viability was assessed using the MTT assay, and levels of ROS and MMP, plus expression of apoptotic protein were analysed.ResultsRotenone induced cell death in SH-SY5Y cells was significantly reduced by DMC pretreatment in a dose-dependent manner, indicating the potent neuroprotective effects of DMC. Rotenone treatment significantly increases the levels of ROS, loss of MMP, release of Cyt-c and expression of pro-apoptotic markers and decreases the expression of anti-apoptotic markers.ConclusionsEven though the results of the present study indicated that the DMC may serve as a potent therapeutic agent particularly for the treatment of neurodegenerative diseases like PD, further pre-clinical and clinical studies are required.
Highlights
Mitochondrial dysfunction and oxidative stress are the main toxic events leading to dopaminergic neuronal death in Parkinson’s disease (PD) and identified as vital objective for therapeutic intercession
Anti- Bax, Bad, Bcl-xL, Bcl-2, caspase-3, caspase-6, and caspase-8, caspase-9, cyt-c anti-bodies were obtained from Cell Signaling Technology, Inc. (Beverly, MA, USA) and β-actin antibody were purchased from Santa Cruz Biotechnology, Inc., (Dallas, TX, USA)
Cells were treated with various concentrations of DMC (5 nM, 10 nM, 20 nM, 50 nM, 100 nM, 200 nM, 500 nM and 1 μM) and rotenone (5 nM, 10 nM, 50 nM, 100 nM and 200 nM) for 24 h and cell survival was determined by MTT assay (Fig. 2a and b)
Summary
Mitochondrial dysfunction and oxidative stress are the main toxic events leading to dopaminergic neuronal death in Parkinson’s disease (PD) and identified as vital objective for therapeutic intercession. Ramkumar et al BMC Complementary and Alternative Medicine (2017) 17:217 the blood-brain barrier due to its high lipophilic nature, transverse the cellular membrane without the need of dopamine transporter. It accumulates and impairs mitochondrial function, mediates oxidative stress and leads to neurodegeneration [5,6,7]. The neuroprotective effect of turmeric can be attributed due to the presence of active polyphenol, curcumin which imparts the characteristic color and properties [12] Both the in vitro and in vivo experiments indicated that the anti-parkinsonic effect of curcumin attributed due to its anti-oxidant [13], mitochondrial protective [14], signal modulating [15], anti-inflammatory [16, 17] and anti-apoptotic properties [18]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
