BACKGROUND: Novel treatment strategies are required to reduce the development of hepatic injury during surgical procedure in which renal ischemia/reperfusion (IR) is inevitable. Remote perconditioning (rPeC) has been proved to reduce the extent of kidney damages induced by renal IR injury. The aim of this study was to determine the protective effect of rPeC against hepatic injury caused by renal ischemia. METHODS: Male rats were subjected to the right nephrectomy and randomized as: sham, no additional intervention; IR, 45 min of left renal pedicle occlusion; rPeC, four cycles of 5-min limb IR administered at the beginning of renal ischemia. After 24-h of reperfusion, the plasma and tissue samples were taken. RESULTS: A significant improvement in hepatic functional injury and oxidative damages were observed in the rPeC group compared to the IR group. However, histological evaluation and plasma levels of TNF-α revealed no significant difference among groups. CONCLUSIONS: It is concluded that rPeC exerted protective effects on renal IR-induced hepatic injury as a remote organ. The protection may be a consequence of the reduction in oxidative stress in the liver. This simple approach may be a promising strategy against IR-induced remote organ damages in the clinical practice (Fig. 4, Ref. 23).
BACKGROUND: Novel treatment strategies are required to reduce the development of hepatic injury during surgical procedure in which renal ischemia/reperfusion (IR) is inevitable. Remote perconditioning (rPeC) has been proved to reduce the extent of kidney damages induced by renal IR injury. The aim of this study was to determine the protective effect of rPeC against hepatic injury caused by renal ischemia. METHODS: Male rats were subjected to the right nephrectomy and randomized as: sham, no additional intervention; IR, 45 min of left renal pedicle occlusion; rPeC, four cycles of 5-min limb IR administered at the beginning of renal ischemia. After 24-h of reperfusion, the plasma and tissue samples were taken. RESULTS: A significant improvement in hepatic functional injury and oxidative damages were observed in the rPeC group compared to the IR group. However, histological evaluation and plasma levels of TNF-α revealed no significant difference among groups. CONCLUSIONS: It is concluded that rPeC exerted protective effects on renal IR-induced hepatic injury as a remote organ. The protection may be a consequence of the reduction in oxidative stress in the liver. This simple approach may be a promising strategy against IR-induced remote organ damages in the clinical practice (Fig. 4, Ref. 23).