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Original Research Article | OPEN ACCESS

Knockdown of TNFAIP1 mitigates sevoflurane-induced cognitive dysfunction by activating CREB/Nrf2 pathway

Jiayu Lu1, Zhenpeng Liu1, Wei He1, Sichao Shao2

1Department of Anesthesiology, The Affiliated Hospital of Beihua University, Jilin City, Jilin Province 132000, China; 2Department of Anesthesiology, Wenzhou Hospital of Integrated Traditional Chinese and Western Medicine, Wenzhou City, Zhejiang Province 325000, China.

For correspondence:-  Sichao Shao   Email: scshao5759@163.com   Tel:+8613587645080

Accepted: 23 June 2022        Published: 31 July 2022

Citation: Lu J, Liu Z, He W, Shao S. Knockdown of TNFAIP1 mitigates sevoflurane-induced cognitive dysfunction by activating CREB/Nrf2 pathway. Trop J Pharm Res 2022; 21(7):1419-1424 doi: 10.4314/tjpr.v21i7.9

© 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 investigate the role of tumor necrosis factor-induced protein 1 (TNFAIP1) and cAMP-responsive element binding protein (CREB)/nuclear factor-erythroid factor 2-related factor 2 (Nrf2) pathway in sevoflurane (SEV)-induced cognitive dysfunction.
Methods: A SEV-induced cognitive dysfunction rat model was developed. Bcl-2, Bax, heme oxygenase-1, Nrf2, p-CREB, and CREB protein levels in rat hippocampal tissue were assessed by western blot. Learning and long-term memory were evaluated using Morris water maze test. Glutathione peroxidase, malondialdehyde, and superoxide dismutase levels in hippocampal tissue were measured by enzyme-linked immunosorbent assay (ELISA). The 2,7-dichlorodihydro-fluorescein diacetate fluorescent assay was used to measure reactive oxygen species, while TUNEL staining was used to assess neuronal cell apoptosis.
Results: Knockdown of TNFAIP1 attenuated SEV-induced learning and long-term memory dysfunction (p < 0.005), oxidative stress (p < 0.005), apoptosis (p < 0.005), and inhibition of the CREB/Nrf2 signaling pathway.
Conclusion: This study demonstrates that knockdown of TNFAIP1 alleviates SEV-induced cognitive dysfunction by reversing inhibition of the CREB/Nrf2 signaling pathway.

Keywords: TNFAIP1, Postoperative cognitive dysfunction, Sevoflurane, CREB, Nrf2

Impact Factor
Thompson Reuters (ISI): 0.6 (2023)
H-5 index (Google Scholar): 49 (2023)

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