Sevoflurane suppresses oxidation-induced stress and inflammatory responses, via promotion of Nrf2-induced antioxidant signaling

Fu, Deshui; Shen, Jufang; Shi, Huimin

doi:10.1080/26895293.2020.1729868

Cited by 4 publications

(2 citation statements)

References 37 publications

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“…Treatment with drugs or small molecules to reduce production of reactive oxygen species [17] or activation of inflammatory networks [18] have been shown to be effectively reduce liver ischemia reperfusion injury. Because sevoflurane was shown to reduce production of reactive oxygen species and inflammatory cytokines, thereby attenuating acute lung injury [19], the role of sevoflurane on liver ischemia reperfusion injury was investigated in this study.…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane alleviates liver ischemia reperfusion injury through inactivation of the TRAF6/NF-κB signaling pathway

Liu¹,

Yuan²,

Rao³

2021

Trop. J. Pharm Res

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Purpose: To evaluate the role and mechanism of action of sevoflurane in liver ischemia reperfusion injury.Methods: Rats were pretreated with sevoflurane and then underwent liver ischemia followed by reperfusion to establish an animal model of liver ischemia reperfusion injury. Pathological changes in liver tissues were investigated by hematoxylin and eosin (H & E) staining, and serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined using a chemistryanalyzer. ELISA was used to determine the levels of myeloperoxidase (MPO), tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β), IL-6, superoxide (SOD), malonaldehyde (MDA), catalase (CAT), and glutathione (GSH).Results: Pathological changes in liver tissue, including sinusoidal congestion, vacuole formation, and infiltration of inflammatory cells and lymphocytes, were identified in rats post-ischemia reperfusion injury. In addition, serum ALT and AST levels increased following ischemia reperfusion injury. However, administration of sevoflurane ameliorated the pathological liver damage and decreased the serum ALTand AST levels induced by ischemia reperfusion. Pro- inflammatory cytokines, such as MPO, TNF-α, IL- 1β, and IL-6 were upregulated in rats following ischemia reperfusion injury, and this upregulation was reversed by sevoflurane administration. Sevoflurane administration also attenuated the ischemia reperfusion-induced increase in MDA and decrease in SOD, CAT, and GSH. Ischemia reperfusionrepressed IκBα protein expression and promoted protein expression of TNF receptor associated factor 6 (TRAF6), phospho (p)-IκBα, and p-p65 in liver tissue. However, sevoflurane reversed the effect of ischemia reperfusion on IκBα, TRAF6, p-IκBα, and p-65 expression.Conclusion: Sevoflurane administration reduced pathological liver injury post-ischemia reperfusion bysuppressing the inflammatory response and oxidative stress through inactivation of the TRAF6/NF-κB pathway.

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Section: Discussionmentioning

confidence: 99%

Sevoflurane alleviates liver ischemia reperfusion injury through inactivation of the TRAF6/NF-κB signaling pathway

Liu¹,

Yuan²,

Rao³

2021

Trop. J. Pharm Res

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“…Generally, sepsis, a major public health burden worldwide, is caused by an unbalanced response from the host to an infection (1,2). Organ failure is a hallmark of sepsis, and it is related to high morbidity and mortality during sepsis (3,4). Among patients with sepsis, ~40% are at risk of developing acute lung injury (ALI) (5).…”

Section: Introductionmentioning

confidence: 99%

Polydatin alleviates sepsis‑induced acute lung injury via downregulation of Spi‑B

Liao,

Li,

Xue

et al. 2023

Biomed Rep

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Sepsis-induced acute lung injury (ALI) is related to the dysregulation of inflammatory responses. Polydatin supplement was reported to exhibit anti-inflammatory effects in several diseases. The present study aimed to investigate the role of polydatin in sepsis-induced ALI. A cecum ligation and puncture (CLP)-induced mouse ALI model was established first and the pathological changes of lung tissues were assessed using hematoxylin and eosin staining. Meanwhile, to mimic sepsis-induced ALI in vitro, pulmonary microvascular endothelial cells (PMVECs) were treated with lipopolysaccharide (LPS). Pro-inflammatory cytokines levels were measured in lung tissues and PMVECs using ELISA. Reverse transcription-quantitative PCR was used to measure the mRNA levels of Spi-B in lung tissues and PMVECs. Moreover, the expression levels of Spi-B, p-PI3K, p-Akt, and p-NF-κB in lung tissues and PMVECs were determined using western blotting. The data revealed that polydatin attenuated CLP-induced lung injury and inhibited sepsis-induced inflammatory responses in mice. Furthermore, polydatin significantly inhibited the expression of Spi-B, p-PI3K, p-Akt, and p-NF-κB in lung tissues of mice subjected to CLP-induced ALI, while this phenomenon was reversed through Spi-B overexpression.Consistently, the anti-inflammatory effect of polydatin was abolished by Spi-B overexpression. Taken together, the current findings revealed that polydatin alleviated sepsis-induced ALI via the downregulation of Spi-B.

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Morphometric analysis of the female reproductive tract: influence of long-term inhalation of trace amounts of sevoflurane

Wang,

Qu,

Yang

et al. 2024

J Mol Histol

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Sevoflurane suppresses oxidation-induced stress and inflammatory responses, via promotion of Nrf2-induced antioxidant signaling

Cited by 4 publications

References 37 publications

Sevoflurane alleviates liver ischemia reperfusion injury through inactivation of the TRAF6/NF-κB signaling pathway

Sevoflurane alleviates liver ischemia reperfusion injury through inactivation of the TRAF6/NF-κB signaling pathway

Polydatin alleviates sepsis‑induced acute lung injury via downregulation of Spi‑B

Morphometric analysis of the female reproductive tract: influence of long-term inhalation of trace amounts of sevoflurane

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