Sevoflurane preconditioning inhibits cardiomyocyte injury induced by oxygen‑glucose deprivation by modulating TXNIP

Ma,Meina; Li,Rui; Sun,Wenbo; Wang,Qi; Yu,Hong; Yu,Hongmei

doi:10.3892/ijmm.2020.4639

Sevoflurane preconditioning inhibits cardiomyocyte injury induced by oxygen‑glucose deprivation by modulating TXNIP

Authors:
- Meina Ma
- Rui Li
- Wenbo Sun
- Qi Wang
- Hong Yu
- Hongmei Yu
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Affiliations: Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, Hebei 061001, P.R. China
Published online on: June 11, 2020 https://doi.org/10.3892/ijmm.2020.4639
Pages: 889-897

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Abstract

The thioredoxin interaction protein (TXNIP) has been reported to be closely related to cell oxidative stress, apoptosis and inflammation. TXNIP is involved in the regulation of oxidative stress in lung and renal injury. However, it is unclear as to whether it participates in the protective effects of sevoflurane preconditioning in cardiomyocyte injury caused by oxidative stress in ischemia. In the present study, H9c2 cardiomyocytes were cultured with 0, 1.5, 2, 3.5, 5 or 6% sevoflurane for 3 h, followed by exposure to oxygen and glucose deprivation. The results demonstrated that oxygen and glucose deprivation induced an increase in TXNIP expression, lactate dehydrogenase (LDH) release, caspase‑3 activity, reactive oxygen species and malondialdehyde production. Preconditioning of the H9c2 cells with 3.5% sevoflurane suppressed TXNIP expression, LDH leakage, caspase‑3 activity, reactive oxygen species and malondialdehyde production, and it promoted cell viability. TXNIP overexpression reversed the effects of 3.5% sevoflurane preconditioning on caspase‑3 activity, reactive oxygen production and cell viability. Furthermore, TXNIP modulated p27 expression via PKB (protein kinase B/AKT) phosphorylation following preconditioning with 3.5% sevoflurane, and oxygen and glucose deprivation. On the whole these findings indicated that sevoflurane preconditioning protected the H9c2 cells against injury induced by oxygen and glucose deprivation by modulating TXNIP, AKT activation and p27 signaling.

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