Sestrin 2 extenuates neuronal ferroptosis induced by sevoflurane through the Nrf2/xCT pathway

LI Fu-jun; JIANG Tao; GUO Li-jia; WANG Shun

doi:10.16766/j.cnki.issn.1674-4152.001949

Volume 19 Issue 6

Jun. 2021

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Article Navigation > Chinese Journal of General Practice > 2021 > 19(6): 917-920,

LI Fu-jun, JIANG Tao, GUO Li-jia, WANG Shun. Sestrin 2 extenuates neuronal ferroptosis induced by sevoflurane through the Nrf2/xCT pathway[J]. Chinese Journal of General Practice, 2021, 19(6): 917-920,. doi: 10.16766/j.cnki.issn.1674-4152.001949

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LI Fu-jun, JIANG Tao, GUO Li-jia, WANG Shun. Sestrin 2 extenuates neuronal ferroptosis induced by sevoflurane through the Nrf2/xCT pathway[J]. Chinese Journal of General Practice, 2021, 19(6): 917-920,. doi: 10.16766/j.cnki.issn.1674-4152.001949

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Sestrin 2 extenuates neuronal ferroptosis induced by sevoflurane through the Nrf2/xCT pathway

doi: 10.16766/j.cnki.issn.1674-4152.001949

LI Fu-jun^{1, 2}
, JIANG Tao³
, GUO Li-jia²
, WANG Shun^{1
,
,}

1.
Acupuncture and Moxibustion Department, Heilongjiang College of Traditional Chinese Medicine, Harbin, Heilongjiang 150036, China

Funds:

2018318

Received Date: 2021-01-29
Available Online: 2022-02-16

Abstract

Abstract

Objective To explore the role of Sestrin 2 (SESN2) in neuronal ferroptosis induced by sevoflurane (SEV) and its possible mechanism. Methods Mouse hippocampal neuron cells HT22 were treated with 0%, 1%, 2% or 4% sevoflurane and iron death inhibitor Ferrostatin-1 (FER-1) for 6 h. SESN2 overexpression vector (SESN2-OE) and corresponding control (NC) were transfected into HT22 cells. The CCK-8 assay was used in detecting cell viability, and the corresponding kit was used in detecting the levels of iron, reactive oxygen species (ROS), malondialdehyde (MDA) and glutathione (GSH). The expression levels of genes and proteins were detected through real-time quantitative PCR (qPCR) and western blot assay. Results qPCR and western blot results showed that SEV treatment significantly inhibited the expression of SESN2 mRNA and protein (t=22.904, 37.432; P < 0.05), whereas transfection with SESN2-OE significantly increased the expression levels of SESN2 mRNA and protein in SEV-treated HT22 cells (t=12.703, 11.687; P < 0.05). SEV treatment significantly increased the levels of iron, ROS and MDA in the HT22 cells (t=29.031, 18.819, 28.054) but significantly reduced the levels of GSH, Nrf2 and xCT (t=14.617, 34.513, 13.836; all P < 0.05). Transfection with SESN2-OE significantly reduced the levels of iron, ROS and MDA in SEV-treated HT22 cells (t=8.342, 9.373, 7.381) but significantly increased the levels of GSH, Nrf2 and xCT (t=12.718, 10.102, 9.814; P < 0.05). Conclusion Sestrin 2 inhibited sevoflurane-induced HT22 neuronal ferroptosis by activating the Nrf2/xCT pathway.
- Sestrin 2,
- Sevoflurane,
- Ferroptosis,
- Neuronal damage

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Sestrin 2 extenuates neuronal ferroptosis induced by sevoflurane through the Nrf2/xCT pathway

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Sestrin 2 extenuates neuronal ferroptosis induced by sevoflurane through the Nrf2/xCT pathway

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