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Purpose: This article aimed to study the role of sevoflurane pre-conditioning in hepatic ischemia-reperfusion and its potential mechanism. Methods: Rat liver ischemia-reperfusion model was constructed. Serum TNF-α, IL-1β, IL-10, and IL-6 concentrations were detected by ELISA. Malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) in liver homogenate were determined. Hematoxylin-Eosin (HE) staining, Tunel, and immunohistochemistry were performed. Ischemia-reperfusion hepatocyte model was established. Cells transfection was conducted. Apoptosis was observed by flow cytometry. Quantitative real-time PCR (qRT-PCR) and Western blotting analysis were used. Results: Compared with I/R group, liver damage degree, liver cell apoptosis, and glucose regulatory protein 78 (Grp78) expression was obviously reduced in rats of SEV group. TNF-α, IL-1β, and IL-6 concentrations were also significantly increased ( P &lt;0.01). MDA and NO concentrations were dramatically lower ( P &lt;0.01) and SOD concentration was significantly higher ( P &lt;0.01). Apoptosis rate, Grp78, PERK, eIF2α, and p-c-JNK/JNK expression was also significantly decreased ( P &lt;0.01). Sevoflurane significantly reduced apoptosis and expression of PERK, eIF2α, p-c-JNK/JNK by inhibiting the expression of Grp78 ( P &lt;0.01). Conclusion: Sevoflurane relieves hepatic ischemia-reperfusion injury by inhibiting the expression of Grp78.

Sevoflurane relieves hepatic ischemia–reperfusion injury by inhibiting the expression of Grp78