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 3 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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Effects of Sevoflurane and Fullerenol C60 on the Heart and Lung in Lower-Extremity Ischemia–Reperfusion Injury in Streptozotocin-Induced Diabetes Mice

Örnek,

Alkan,

Erel

et al. 2024

Medicina

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Background and Objectives: Lower-extremity ischemia–reperfusion injury can induce distant organ ischemia, and patients with diabetes are particularly susceptible to ischemia–reperfusion injury. Sevoflurane, a widely used halogenated inhalation anesthetic, and fullerenol C60, a potent antioxidant, were investigated for their effects on heart and lung tissues in lower-extremity ischemia–reperfusion injury in streptozotocin (STZ)-induced diabetic mice. Materials and Methods: A total of 41 mice were divided into six groups: control (n = 6), diabetes–control (n = 7), diabetes–ischemia (n = 7), diabetes–ischemia–fullerenol C60 (n = 7), diabetes–ischemia–sevoflurane (n = 7), and diabetes–ischemia–fullerenol C60–sevoflurane (n = 7). Diabetes was induced in mice using a single intraperitoneal dose of 55 mg/kg STZ in all groups except for the control group. Mice in the control and diabetes–control groups underwent midline laparotomy and were sacrificed after 120 min. The DIR group underwent 120 min of lower-extremity ischemia followed by 120 min of reperfusion. In the DIR-F group, mice received 100 μg/kg fullerenol C60 intraperitoneally 30 min before IR. In the DIR-S group, sevoflurane and oxygen were administered during the IR procedure. In the DIR-FS group, fullerenol C60 and sevoflurane were administered. Biochemical and histological evaluations were performed on collected heart and lung tissues. Results: Histological examination of heart tissues showed significantly higher necrosis, polymorphonuclear leukocyte infiltration, edema, and total damage scores in the DIR group compared to controls. These effects were attenuated in fullerenol-treated groups. Lung tissue examination revealed more alveolar wall edema, hemorrhage, vascular congestion, polymorphonuclear leukocyte infiltration, and higher total damage scores in the DIR group compared to controls, with reduced injury parameters in the fullerenol-treated groups. Biochemical analyses indicated significantly higher total oxidative stress, oxidative stress index, and paraoxonase-1 levels in the DIR group compared to the control and diabetic groups. These levels were lower in the fullerenol-treated groups. Conclusions: Distant organ damage in the lung and heart tissues due to lower-extremity ischemia–reperfusion injury can be significantly reduced by fullerenol C60.

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

Cited by 3 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

Effects of Sevoflurane and Fullerenol C60 on the Heart and Lung in Lower-Extremity Ischemia–Reperfusion Injury in Streptozotocin-Induced Diabetes Mice

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