Icaritin attenuates 6-OHDA-induced MN9D cell damage by inhibiting oxidative stress
Xinyu Zhou,
Nanqu Huang,
Xiaoyi Hou,
Li Zhu,
Yiman Xie,
Zhisheng Ba,
Yong Luo
Affiliations
Xinyu Zhou
Department of Neurology, The First People’s Hospital of Zunyi & Third Affiliated Hospital of Zunyi Medical University, Zunyi, Ghuizhou, China
Nanqu Huang
National Drug Clinical Trial Institution, The First People’s Hospital of Zunyi & Third Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, China
Xiaoyi Hou
Department of Neurology, The First People’s Hospital of Zunyi & Third Affiliated Hospital of Zunyi Medical University, Zunyi, Ghuizhou, China
Li Zhu
School of Medicine and Technology, Zunyi Medical University, Zunyi, Guizhou, China
Yiman Xie
Department of Neurology, The First People’s Hospital of Zunyi & Third Affiliated Hospital of Zunyi Medical University, Zunyi, Ghuizhou, China
Zhisheng Ba
National Drug Clinical Trial Institution, The First People’s Hospital of Zunyi & Third Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, China
Yong Luo
Department of Neurology, The First People’s Hospital of Zunyi & Third Affiliated Hospital of Zunyi Medical University, Zunyi, Ghuizhou, China
Background We assessed whether ICT can alleviate 6-OHDA-induced cell damage via inhibition of oxidative stress by evaluating the protective effect of icaritin (ICT) against 6-hydroxydopamine (6-OHDA)-induced MN9D cell damage and further determined the mechanism by which ICT reduces oxidative stress. Methods MN9D cells were treated with 6-OHDA, to study the mechanism underlying the neuroprotective effect of ICT. MN9D cell damage was assessed by the CCK-8 assay, flow cytometry was performed to measure the content of reactive oxygen species (ROS) in cells, a superoxide dismutase (SOD) kit was used to evaluate SOD activity, and Western blotting was used to measure the expression of α-synuclein (α-Syn), Tyrosine hydroxylase (TH), nuclear factor erythroid-2 related factor 2 (Nrf2), and heme oxygenase-1 (HO-1). Results ICT reduced damage to MN9D cells induced by 6-OHDA. ICT increased SOD activity and TH expression and reduced ROS production and α-Syn expression. ICT promoted the translocation of Nrf2 from the cytoplasm to the nucleus and further increased the protein expression of HO-1. Conclusions ICT protects against 6-OHDA-induced dopaminergic neuronal cell injury by attenuating oxidative stress, and the mechanism is related to modulate the activities of Nrf2, HO-1 protein, and SOD.
