Journal of Shandong University (Health Sciences) ›› 2019, Vol. 57 ›› Issue (3): 25-30.doi: 10.6040/j.issn.1671-7554.0.2018.877

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Effects of sevoflurane preconditioning on silent information regulator of transcription 3 expression and acetylation in H9C2 cardiomyocytes after hypoxia/reoxygenation

XIONG Chao, LIU Li, FENG Jianguo, WEI Jicheng   

  1. Department of Anesthesiology, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China
  • Published:2022-09-27

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Abstract: Objective To investigate the effects of sevoflurane preconditioning on silent information regulator of transcription 3(SIRT3)expression and the acetylation of H9C2 cardiomyocytes after hypoxia/reoxygenation. Methods Rat H9C2 cardiomyocytes were randomly divided into control group, hypoxia/reoxygenation group and sevoflurane pretreatment group. Cells without any treatment served as control group. Hypoxia/reoxygenation models were prepared in a hypoxia incubator, in which cells were exposed to 2 h hypoxia followed by 2 h reoxygenation. Cells in the sevoflurane pretreatment group were treated with 2.5% sevoflurane for 1 h before hypoxia/reoxygenation processing. The cell survival 山 东 大 学 学 报 (医 学 版)57卷3期 -熊超,等.七氟醚预处理对H9C2心肌细胞缺氧/复氧后转录沉默信息调节器3的表达及乙酰化水平的影响 \=-was detected with methylthiazolyltetrazolium(MTT)assay. Mitochondrial membrane potential was examined with JC-1 fluorescence probe. The acetylation of proteins, especially that of mitochondrial protein, SIRT3 expression, and mitophagy level were detected with Western blotting. Results Compared with the control group, the hypoxia/reoxygenation group had decreased expression of SIRT3(0.78±0.04 vs 1.04±0.06), increased acetylation level of proteins(1.72±0.06 vs 0.98±0.03)and mitochondrial protein(0.96±0.03 vs 0.45±0.03)(P<0.05), decreased cell survival ［(48.2±0.4)% vs 100%］, decreased mitochondrial membrane potential(1.72±0.14 vs 2.83±0.11), and increased mitophagy level(P<0.05). Compared with the hypoxia/reoxygenation group, the sevoflurane pretreatment group had increased expression of SIRT3(0.93±0.03 vs 0.78±0.04), decreased acetylation level of proteins(1.34±0.05 vs 1.72±0.06)and mitochondrial protein(0.65±0.04 vs 0.96±0.03)(P<0.05), increased cell survival ［(65.80±1.53)% vs (48.20±0.40)%］ and mitochondrial membrane potential(2.33±0.12 vs 1.72±0.14), and decreased mitophagy level(P<0.05). Conclusion Sevoflurane pretreatment is capable of elevating the expression of SIRT3 and downregulating the acetylation of H9C2 cells after hypoxia/reoxygenation injury, which might be the molecular mechanism underlying the protective effects of sevoflurane on cardiomyocytes.

Key words: Sevoflurane preconditioning, Acetylization, Silent information regulator of transcription 3, Mitophagy, Hypoxia/reoxygenation

CLC Number: 

  • R197.1
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