Effect of silencing Fisl gene on METH-induced proliferative capacity, mitochondrial membrane potential and ultrastructure of SH-SY5Y cells cultured in vitro / 中国药理学通报
Chinese Pharmacological Bulletin
;
(12): 1725-1730, 2019.
Artigo
em Chinês
| WPRIM
| ID: wpr-857079
ABSTRACT
Aim To evaluate the role of fisson I (Fisl) in methamphetamine (METH)-induced injur)' of human neuroblastoma (SH-SY5Y) cells cultured in vitro. Methods SH-SY5Y cells cultured in vitro were divided into different groups by the group design method∗. unsilent groups, silent negative groups and silent groups. Different concentrations of METH induced SH-SY5 Y cells in each group for 24 hours. The expression level of Fisl was detected by Western blot. The effect of METH on the proliferative capacity of SH-SY5Y cells was analyzed by CCK-8 cytotoxicity proliferation assay. The MMP level of METH on SH-SY5Y cells was detected by mitochondrial membrane potential detection kit (JC-1). The effect of METH on the mitochondrial ultrastructure of SH-SY5Y cells was observed by transmission electron microscopy. Results In unsilent group, silent negative group and silent group, the expression level of Fisl increased (P < 0. 05) and the proliferative capacity decreased (P < 0. 05) , and the MMP levels decreased (P <0. 05) with the increase of the concentration of SH-SY5Y cells induced by METH. Compared with the same concentration in unsi-lent group and silent negative group, in silent group, the expression level of Fisl in SH-SY5Y cells de-creased (P < 0. 05) , the proliferative capacity increased (P<0. 05) , and the MMP level increased (P < 0. 05). Compared with control group, 2. 0 mmol • L"1 METH induced unsilent groups, silent negative groups and silent groups, and transmission electron microscopy showed the increase in the mitochondrial small globular structure (P < 0. 01). Conclusion Fisl may play a key role in METH-induced injury of SH-SY5Y cells cultured in vitro.
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Índice:
WPRIM (Pacífico Ocidental)
Idioma:
Chinês
Revista:
Chinese Pharmacological Bulletin
Ano de publicação:
2019
Tipo de documento:
Artigo
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