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Original Research Article | OPEN ACCESS

Sevoflurane induces ho-1-mrna expression by regulating P13K/Akt/P70S6K signaling pathway and affects neuronal apoptosis

Zhiqiang Lu1, Yan Wei2, Jiandang Xu1, Yinghua Tang1

1Department of Anesthesiology, Shanghai No. 8 People's Hospital, Shanghai 200235, China; 2Department of Anesthesiology, Shanghai Pudong New Area People's Hospital, Shanghai 201299, China.

For correspondence:-  Yinghua Tang   Email: ri5wvb@163.com

Accepted: 13 May 2022        Published: 30 June 2022

Citation: Lu Z, Wei Y, Xu J, Tang Y. Sevoflurane induces ho-1-mrna expression by regulating P13K/Akt/P70S6K signaling pathway and affects neuronal apoptosis. Trop J Pharm Res 2022; 21(6):1161-1167 doi: 10.4314/tjpr.v21i6.4

© 2022 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To determine the effect of sevoflurane (SE) on neuronal apoptosis, and the mechanism involved.
Methods: Sixty healthy male Sprague-Dawley rats were assigned to control, model and SE groups. Sham surgery was performed in control group, while middle cerebral artery infarction (MCAO) was established in model group. The expression of HO-1 mRNA was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Apoptosis, autophagy and protein content of P13K/Akt/P70S6K signaling pathway were assessed by Western blot assay.
Results: Apoptosis was significantly lower in SE rats, relative to model rats. There were markedly higher protein levels of LC3 II / I, beclin-1, bad, Bcl-2 and caspase-3 in model and SE groups than in control rats (p < 0.05). The HO-1 mRNA was significantly up-regulated in model and SE groups, relative to controls, but it was significantly up-regulated in SE group, relative to model rats (p < 0.05). The expression levels of phosphorylated proteins of the P13K/Akt /P70S6K signal-related proteins in model and SE groups were significantly up-regulated, relative to control, but elevated in SE mice, when compared to model mice (p < 0.05).
Conclusion: SE improves the behavior of MCAO rats, reduces cerebral infarction, and inhibits apoptosis and autophagy of nerve cells by regulating autophagy and apoptosis-related proteins through a mechanism that may be related to the induction of HO-1-mRNA expression by regulating P13K/Akt /P70S6K signal pathway. This provides new insights for the development of anti-neuronal apoptosis drugs.

Keywords: Sevoflurane, P13K/Akt/P70S6K signaling pathway, HO-1-mRNA, Neuronal cells, Apoptosis

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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