科研之友
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摘要
Aim To investigate the effect of circRNA- 32011 on myocardial apoptosis induced by arsenic triox- ide (ATO).Methods Primary cardioniyocytes of suckling neonate mouse were treated with ATO ( final concentration 10 (xniol ? L_1 ) for 24 h.Then cell via?bility was measured by M IT assay.The mKNA expres?sion levels of Bel-2/ Bax and circRNA-3201 I were de?tected by KT-PCK.Bcl-2/Bax protein expression lev?els were detected by Western blot.Overexpression and knock down circHNA-32011 respectively by plasmid and siHNA were used to verify its function in ATO-in- duced cardiomyocyte apoptosis.Results Myocardial cell viability decreased, Bel-2 expression significantly decreased while Bax expression increased in ATO group compared with the control group.CircKNA- 32011 was down-regulated in ATO ineuhated cardio?niyocytes.Ovcrex press ion of circRNA-32011 in ATO- incubated cardioniyocytes increased myocardial cell vi?ability and Bel-2 expression and decreased the expres?sion of Bax.Knockdown of circRNA-32011 could fur?ther reduce cardiomyoevte activity and Bel-2 expression and increase the experssion of Bax induced by ATO.Conclusions CircRNA-32011 protects cardiac myo?cytes from apoptosis induced by arsenic trioxide, which may provide a new potential therapeutic strategy for ATO-induced myocardial injury. ? 2022 Publication Centre of Anhui Medical University.
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