| Autor: |
Xinyu Zhou, Nanqu Huang, Xiaoyi Hou, Li Zhu, Yiman Xie, Zhisheng Ba, Yong Luo |
| Jazyk: |
angličtina |
| Rok vydání: |
2022 |
| Předmět: |
|
| Zdroj: |
PeerJ, Vol 10, p e13256 (2022) |
| Druh dokumentu: |
article |
| ISSN: |
2167-8359 |
| DOI: |
10.7717/peerj.13256 |
| Popis: |
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. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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