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Effect of Evodiamine on 6-Hydroxydopamine Induced Damage of Parkinson's Disease Cell Model by Modulating MicroRNA-9-5p

Author(s): Xinyu Chen, Jing Shao, Ruoran Li, Shuang Shao, Xilu Zhang, Mingming Ma, Jing Sun and Na Li*
Department of Medicine, Qiqihar First Hospital, 1Department of Neurology, First South Campus, 2Department of Neurology, First North Campus, 3Department of Neurology, Fifth North Campus, Qiqihar First Hospital, Qiqihar, Heilongjiang 161005, China

Correspondence Address:
Na Li, Department of Neurology, Fifth North Campus, Qiqihar First Hospital, Qiqihar, Heilongjiang 161005, China, E-mail:

To explore the effect of evodiamine on Parkinson’s disease and its possible mechanism. 6-hydroxydopamine challenged SK-N-SH cells were adopted to mimic Parkinson’s disease condition in vitro. Levels of proteins and genes were tested using Western blot and quantitative reverse transcription-polymerase chain reaction. Oxidative stress was evaluated by detecting the expression of lactate dehydrogenase and glutathione. Enzyme-linked immunosorbent assay analysis and flow cytometry were applied for the examination of inflammatory reaction and apoptosis rate. Evodiamine treatment could dosedependently inhibit lactate dehydrogenase activity and cell apoptosis, reduced the levels of inflammatory factors, but elevated glutathione content in 6-hydroxydopamine-challenged SK-N-SH cells. Evodiamine exposure led to the decline of microRNA-9-5p content. Inhibition of microRNA-9-5p was able to protect against 6-hydroxydopamine stimulated oxidative stress, elevation of apoptosis and inflammatory factors in cells. Besides that, boosting microRNA-9-5p attenuated the protective functions of evodiamine on 6-hydroxydopamine stimulated SK-N-SH cells. Evodiamine could inhibit 6-hydroxydopamine induced oxidative, inflammatory and apoptotic injury in the Parkinson’ s disease cell model via microRNA-9-5p.

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