Abstract
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.
Highlights
Liver ischemia reperfusion injury is a complicated pathophysiological process that occurs during liver transplantation and tissue resection surgery [1]
The results showed that ischemia reperfusion induced pathological changes in liver tissue as demonstrated by hepatocellular swelling, sinusoidal congestion, and infiltration of inflammatory cells and lymphocytes (Figure 1 A)
ELISA data showed that ischemia reperfusion increased MPO activity (Figure 2 A) and increased levels of the proinflammatory cytokines tumor necrosis factor-α (TNF-α) (Figure 2 B), IL-1β (Figure 2 C), and IL-6 (Figure 2 D) in liver tissue
Summary
Liver ischemia reperfusion injury is a complicated pathophysiological process that occurs during liver transplantation and tissue resection surgery [1]. The protective effect of sevoflurane against liver ischemia reperfusion injury has been investigated in animal models. The mechanism by which sevoflurane exerts its protective effect on liver ischemia reperfusion injury remains unclear and requires further study. The effects and mechanism of sevoflurane treatment on liver inflammation and oxidative stress induced by ischemia/reperfusion were investigated. Myeloperoxidase (MPO), tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β), and IL-6 levels in liver tissues were measured using commercial assay kits (Sigma Aldrich, St. Louis, MO, USA). Proteins were extracted from liver tissues using the ProteoPrep Total Extraction Sample Kit (Sigma-Aldrich) and protein concentrations were determined using a BCA protein assay kit (Beyotime, Shanghai, China).
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