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Dexmedetomidine protects SH‐SY5Y cells against MPP + ‐induced declining of mitochondrial membrane potential and cell cycle deficits
Author(s) -
Chen Yaohua,
Chen Cheng,
Song Dan,
Liu Tingting,
Cheng Oumei
Publication year - 2021
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.15252
Subject(s) - sh sy5y , apoptosis , membrane potential , cell cycle , agonist , microbiology and biotechnology , cell cycle checkpoint , pharmacology , reactive oxygen species , flow cytometry , biology , receptor , mitochondrion , chemistry , cell culture , biochemistry , neuroblastoma , genetics
Dexmedetomidine (Dex), an adrenergic α2 receptor agonist, is commonly used in deep‐brain stimulation surgery for Parkinson's disease (PD). However, there is evidence that the use of anaesthetics may accelerate the progression of neurodegenerative diseases. The effect of Dex on PD remains unclear. Here, we cultured the all‐trans‐retinoicacid (ATRA) differentiated SH‐SY5Y cells in vitro and then treated with MPP + (1.5mM) with or without Dex (10nM) or Dex combined with Atipamezole (Ati,100nM, adrenergic α2 receptor inhibitor). The ratio of apoptotic cells, mitochondrial membrane potential (Δψm), reactive oxygen species (ROS), cell cycle and apoptotic markers (Cleaved caspase‐3, 9) were analysed by flow cytometry and immunofluorescence. We found that the levels of apoptotic ratio and cleaved caspase‐3, 9 increased, ROS accumulated, and mitochondrial membrane potential decreased after MPP+treatment, while these changes were partially reversed by Dex. Dex also prevented MPP + induced cell arrest by increasing G1 phase cells, decreasing S phase cells, and decreasing the expression of cyclinD1 and Cdk4. Moreover the effects of Dex were partially reversed by Ati. These findings reveal that Dex attenuated MPP + ‐induced apoptosis of SH‐SY5Y cells by preventing the loss of Δψm, reducing ROS, and regulating the cell cycle. Our findings indicated that Dex is more likely to be a potential drug for the treatment of PD.