Co-enzyme Q10 protects primary chicken myocardial cells from heat stress by upregulating autophagy and suppressing the PI3K/AKT/mTOR pathway
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In this study, we investigated the function of co-enzyme Q10 (Q10) in autophagy of primary chicken myocardial cells during heat stress. Cells were treated with Q10 (1 μΜ, 10 μΜ, and 20 μM) before exposure to heat stress. Pretreatment of chicken myocardial cells with Q10 suppressed the decline in cell viability during heat stress and suppressed the increase in apoptosis during heat stress. Treatment with 20 μM Q10 upregulated autophagy-associated genes during heat stress. The expression of LC3-II was highest in cells treated with 20 μM Q10. Pretreatment with Q10 decreased reactive oxygen species (ROS) levels during heat stress. The number of autophagosomes was significantly increased by 20 μM Q10 treatment, as demonstrated by electron microscopy or monodansylcadaverine (MDC) fluorescence. SQSTM1 accumulation was diminished by Q10 treatment during heat stress, and the number of LC3II puncta was increased. Treatment with 20 μM Q10 also decreased the activation of the PI3K/Akt/mTOR pathway. Our results showed that co-enzyme Q10 can protect primary chicken myocardial cells by upregulating autophagy and suppressing the PI3K/Akt/mTOR pathway during heat stress.
KeywordsCo-enzyme Q10 Heat stress Autophagy Myocardial cells Chicken
This work was supported by the National Natural Science Foundation of China (grant numbers 31602027, 31672520), the Jiangsu Natural Science Foundation of China (grant number BK20160732), the China Postdoctoral Science Foundation (grant number 2016M591860), the Priority Academic Program Development of Jiangsu Higher Education Institutions, Graduate Research, and the Innovation Projects in Jiangsu Province.
Compliance with ethical standards
The study protocol was approved by the Animal Care and Use Committee of Nanjing Agricultural University (Nanjing, China).
Conflict of interest
The authors declare that they have no competing interest.
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