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Icariin reduces Glu‐induced excitatory neurotoxicity via antioxidative and antiapoptotic pathways in SH‐SY5Y cells
Author(s) -
Zheng Xing Xing,
Li Ying Chun,
Yang Kai Lin,
He Zhou Xiao,
Wang Zhao Liang,
Wang Xing,
Jing Hui Ling,
Cao Yan Jun
Publication year - 2021
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.7057
Subject(s) - icariin , neurotoxicity , viability assay , sh sy5y , oxidative stress , apoptosis , reactive oxygen species , pharmacology , membrane potential , chemistry , p38 mitogen activated protein kinases , glutamate receptor , microbiology and biotechnology , biology , biochemistry , mapk/erk pathway , signal transduction , cell culture , toxicity , medicine , receptor , alternative medicine , organic chemistry , pathology , genetics , neuroblastoma
Excessive glutamate (Glu) can lead to significant effects on neural cells through the generation of neurotoxic or excitotoxic cascades. Icariin (ICA) is a main active ingredient of Chinese Medicine Berberidaceae epimedium L., and has many biological activities, such as antiinflammation, antioxidative stress, and anti‐depression. This study aims to evaluate the effect of ICA on Glu‐induced excitatory neurotoxicity of SH‐SY5Y cells. The cell viability assay was evaluated by the CCK‐8 assay. The apoptosis, reactive oxygen species (ROS), and mitochondrial membrane potential were assessed by flow cytometry. Intracellular Ca 2+ concentration was determined by using the fluorescent probe Fluo‐3. Protein expression was detected by western blotting analysis. ICA can significantly enhance the SH‐SY5Y cell viability reduced by Glu. At the same time, ICA can significantly reduce apoptosis, ROS, nitric oxide (NO) levels, and intracellular Ca 2+ concentration, and significantly inhibit the increase of mitochondrial membrane potential. In addition, ICA significantly increased the expression of P47phox and iNOS, decreased p‐JNK/JNK, p‐P38/P38, Bax/Bcl‐2, active caspase‐3, and active caspase‐9. These results indicate that ICA may reduce the excitatory neurotoxicity of Glu‐induced SH‐SY5Y cells through suppression of oxidative stress and apoptotic pathways, suggesting that ICA could be a potential therapeutic candidate for neurological disorders propagated by Glu toxicity.