Publication:
Urolithin A attenuates bupivacaine-induced neurotoxicity in SH-SY5Y cells by regulating the SIRT1-activated PI3K/AKT pathway

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Liu-39-1485-1492-2024 (2).pdf(1.74 MB)
Date
2024
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Authors
Liu, Bin ; Wei, Yuan
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-18-737
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info:eu-repo/semantics/article
Description
Abstract
Urolithin A (UroA) is well-recognized for its anti-oxidative, anti-inflammatory, and immuno-modulatory potentials and has been proven to have neuroprotective effects. Nevertheless, the potential of UroA on bupivacaine (BUP)-induced neurotoxicity has never been reported. Using SH-SY5Y cells to establish a cell model, it was revealed that BUP stimulated cell viability reduction, LDH release increase, and suppression of SIRT1-activated PI3K/AKT signaling in SH-SY5Y cells, whereas UroA treatment caused an effective abrogation of the effects of BUP. Besides, SIRT1 overexpression caused an enhancement in the activity of PI3K/AKT signaling in BUP and UroA co-treated cells, indicating that SIRT1 mediated the activity of PI3K/AKT signaling. Moreover, UroA inhibited BUP-induced apoptosis, oxidative stress, and inflammatory responses in SH-SY5Y cells. However, the effects of UroA on BUP-induced neurotoxicity were all abated by inhibiting SIRT1 or PI3K/AKT signaling through EX527 or LY294002. In conclusion, UroA protected SH-SY5Y cells against BUP-induced injuries through PI3K/AKT signaling in a SIRT1-dependent manner.
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Urolithin A , SIRT1 , PI3K/AKT , Bupivacaine , Neurotoxicity
Citation
Histology and Histopathology Vol. 39, nº11 (2024)
URI
http://hdl.handle.net/10201/145021
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Histology and histopathology Vol.39,nº11 (2024)
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