TY - JOUR
T1 - Neuroprotective effect of Demethoxycurcumin, a natural derivative of Curcumin on rotenone induced neurotoxicity in SH-SY 5Y Neuroblastoma cells
AU - Ramkumar, Muthu
AU - Rajasankar, Srinivasagam
AU - Gobi, Veerappan Venkatesh
AU - Dhanalakshmi, Chinnasamy
AU - Manivasagam, Thamilarasan
AU - Justin Thenmozhi, Arokiasamy
AU - Essa, Musthafa Mohamed
AU - Kalandar, Ameer
AU - Chidambaram, Ranganathan
N1 - Publisher Copyright:
© 2017 The Author(s).
PY - 2017/4/18
Y1 - 2017/4/18
N2 - Background: 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. This study investigated the neuro-protective effects of the demethoxycurcumin (DMC), a derivative of curcumin against rotenone induced neurotoxicity. Methods: SH-SY5Y neuroblastoma cells are divided into four experimental groups: untreated cells, cells incubated with rotenone (100nM), cells treated with DMC (50nM)+rotenone (100nM) and DMC alone treated. 24h after treatment with rotenone and 28h 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. Results: Rotenone 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. Conclusions: Even 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.
AB - Background: 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. This study investigated the neuro-protective effects of the demethoxycurcumin (DMC), a derivative of curcumin against rotenone induced neurotoxicity. Methods: SH-SY5Y neuroblastoma cells are divided into four experimental groups: untreated cells, cells incubated with rotenone (100nM), cells treated with DMC (50nM)+rotenone (100nM) and DMC alone treated. 24h after treatment with rotenone and 28h 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. Results: Rotenone 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. Conclusions: Even 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.
KW - Apoptosis
KW - Demethoxycurcumin
KW - Neurodegenerative diseases
KW - Oxidative stress
KW - Rotenone
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UR - http://www.scopus.com/inward/citedby.url?scp=85018385142&partnerID=8YFLogxK
U2 - 10.1186/s12906-017-1720-5
DO - 10.1186/s12906-017-1720-5
M3 - Article
C2 - 28420370
AN - SCOPUS:85018385142
SN - 1472-6882
VL - 17
JO - BMC Complementary and Alternative Medicine
JF - BMC Complementary and Alternative Medicine
IS - 1
M1 - 217
ER -