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Original Research Article | OPEN ACCESS

HSF-1 attenuates isoflurane-induced cognitive dysfunction by inhibiting TLR2 expression

Xu Jia1, Xuezhu Huang1 , Mingda Duan2, Wei Qiu1, Xuanbo Zhang1, Xin Wang3

1Department of Anesthesiology, Affiliated Hospital of Yanbian University, Yanji City, Jilin Province 133000, China; 2Department of Anesthesiology, Hainan Hospital of General Hospital of PLA, Sanya, Hainan Province 572013, China; 3Department of Otolaryngology, Hainan Hospital of General Hospital of PLA, Sanya, Hainan Province 572013, China.

For correspondence:-  Xuezhu Huang   Email: xzhuang6664@163.com   Tel:+864332660157

Accepted: 1 September 2022        Published: 30 September 2022

Citation: Jia X, Huang X, Duan M, Qiu W, Zhang X, Wang X. HSF-1 attenuates isoflurane-induced cognitive dysfunction by inhibiting TLR2 expression. Trop J Pharm Res 2022; 21(9):1829-1835 doi: 10.4314/tjpr.v21i9.3

© 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 regulatory effects of heat shock factor 1 (HSF-1) in the progression of postoperative cognitive dysfunction (POCD).
Methods: Isoflurane (ISO)-induced POCD model in rats was established to determine the role of HSF-1 in POCD. Morris water maze test was used to evaluate the learning and memory abilities of the POCD rats while mRNA and protein levels of HSF-1 were determined by RNA extraction/quantitative real-time polymerase chain reaction (RT-qPCR) and western blot analysis, respectively.
Results: The mRNA and protein levels of HSF-1 were significantly reduced in ISO model, but OE-HSF-1 treatment significantly elevated HSF-1 level (p < 0.05). ISO treatment also significantly decreased escape latency but increased the decreased target quadrant of the rats, while HSF-1 upregulation reversed these effects (p < 0.05). Additionally, HSF-1 alleviated ISO-induced hippocampal injury, improved ISO-induced hippocampal inflammation, and inhibited ISO-induced hippocampal apoptosis. Furthermore, HSF-1 was modulated by POCD via TLR2/NF-κB pathway (p < 0.05).
Conclusion: HSF-1 attenuates ISO-induced cognitive dysfunction by suppressing TLR2 expression. This activity provides a potential strategy to prevent POCD via HSF-1.

Keywords: Heat shock factor 1, Isoflurane, Cognitive dysfunction, Hippocampal inflammation

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

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