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Oxidative stress, caused by renal ischemia reperfusion (IR)/hypoperfusion, is one of the main causes of acute kidney injury (AKI). Previous studies have demonstrated that sevoflurane (SEV) protects organs from the damage caused by oxidative stress. In the present study, mice were randomly assigned to a sham operation group (Sham), IR-vehicle group (IR+ vehicle), IR + SEV low-dose preconditioning group and an IR + SEV high-dose preconditioning group. The effect of SEV on nuclear factor E2-related factor 2 (Nrf2), a key regulatory protein of the endogenous antioxidant defense system and, consequently oxidative stress, inflammation and apoptosis-related factors, were all quantified using commercial kits or by western blotting. SEV preconditioning was demonstrated to ameliorate kidney injury as a result of decreased blood urine nitrogen and serum creatinine levels, activated Nrf2 expression in the kidney and decreased oxidative stress and inflammatory index levels an AKI mouse model. SEV preconditioning also protected injured kidney via the downregulation of caspase-3 protein expression levels. In addition, using the Nrf2 inhibitor, Brusatol, significantly abolished the SEV preconditioning renal protective effect. Using an in vitro HK-2 cell model of hypoxia/reoxygenation, it was also demonstrated that Nrf2 pathway activation was necessary for SEV to exert its beneficial effect for tubular cell injury caused by hypoxia/reoxygenation. These results indicated that SEV may protect against renal injury caused by IR via Nrf2 upregulation.

Summary A new gelatin‐protocatechuic acid (PCA) film with Escherichia coli O157:H7 phage JN01 was developed and characterised. After incorporated with JN01, swelling value, water vapour permeability, water solubility and elongation at break of gelatin‐PCA film were not significantly different. The addition of JN01 increased b value and transparency of film, while it decreased L value, a value and tensile strength of film. Moreover, the gelatin‐PCA‐JN01 film presented antioxidant activity of 60.07%. Furthermore, JN01 could be steadily released from gelatin‐JN01 and gelatin‐PCA‐JN01 films in aqueous solution, and their release rates were 7.56% and 0.12% after 11 h, respectively. The microstructure analysis showed that JN01 particles were clustered and uniformly distributed in film, and the aggregation would be attenuated in the presence of PCA. Meanwhile, E. coli O157:H7 counts were 1.13 log10CFU mL−1 and 0.45 log10CFU mL−1 lower in gelatin‐JN01 and gelatin‐PCA‐JN01 films compared with pure gelatin film in vitro at 4 °C for 24 h, respectively. After stored at 4 °C for 7 days, Escherichia coli O157:H7 counts were 1.00 log10CFU g−1 and 0.80 log10CFU g−1 lower in beef packed with these two gelatin films, compared with beef without gelatin film, respectively. In conclusion, the developed gelatin‐PCA‐JN01 film has potential application in food preservation.

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