Abstract

Purpose:To evaluate the effects of splenic ischemic preconditioning (sIPC) on oxidative stress induced by hepatic ischemia-reperfusion in rats.Methods:Fifteen male Wistar rats were equally divided into 3 groups: SHAM, IRI and sIPC. Animals from IRI group were subjected to 45 minutes of partial liver ischemia (70%). In the sIPC group, splenic artery was clamped in 2 cycles of 5 min of ischemia and 5 min of reperfusion (20 min total) prior to hepatic ischemia. SHAM group underwent the same surgical procedures as in the remaining groups, but no liver ischemia or sIPC were induced. After 1h, hepatic and splenic tissue samples were harvested for TBARS, CAT, GPx and GSH-Rd measurement.Results:sIPC treatment significantly decreased both hepatic and splenic levels of TBARS when compared to IRI group (p<0.01). Furthermore, the hepatic and splenic activities of CAT, GPx and GSH- Rd were significantly higher in sIPC group than in IRI group.Conclusion:sIPC was able to attenuate hepatic and splenic IRI-induced oxidative stress.

Highlights

  • Ischemia-reperfusion injury (IRI) refers to an exacerbation of cellular damage following restoration of blood flow and oxygen delivery to hypoxic tissues[1]

  • When applied to tissues that are not directly exposed to ischemia, Ischemic preconditioning (IPC) can provide cellular protection against a distant organ IRI, which is known as remote ischemic preconditioning (RIPC) procedure[4]

  • IRI group had significantly higher hepatic (45.29 ± 3.18) and splenic (43.74 ± 2.14) levels of thiobarbituric acid reactive substances (TBARS) when compared to SHAM group

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Summary

Introduction

Ischemia-reperfusion injury (IRI) refers to an exacerbation of cellular damage following restoration of blood flow and oxygen delivery to hypoxic tissues[1]. It is a common cause of liver dysfunction after major resection/ transplantation[2] and contributes to a high morbidity and mortality. Ischemic preconditioning (IPC), defined as multiple brief ischemic episodes before a sustained ischemic insult[4], has been shown to attenuate experimental liver IRI by decreasing oxidative damage, inflammation, apoptosis and microcirculatory dysfunction[5]. When applied to tissues that are not directly exposed to ischemia, IPC can provide cellular protection against a distant organ IRI, which is known as remote ischemic preconditioning (RIPC) procedure[4]. Different anatomical sites have been successfully used to perform RIPC among rodent models of hepatic IRI, such as hindlimb[6] and superior mesenteric artery[7], but other locations may ensure favorable outcomes as well

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