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Icaritin attenuates 6-OHDA-induced MN9D cell damage by inhibiting oxidative stress
Xinyu Zhou1, Nanqu Huang2, Xiaoyi Hou1
1Department 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.
