Protection of Liver as a Remote Organ after Renal Ischemia-Reperfusion Injury by Renal Ischemic Postconditioning

Abstract

This study was designed to investigate the protective effects of local renal ischemic postconditioning (POC) on liver damage after renal ischemia-reperfusion (IR) injury. Male rats were divided into three groups (n = 8). They underwent a right nephrectomy before induction of 45 minutes of left kidney ischemia or sham operation. POC was performed by four cycles of 10 seconds of ischemia and 10 seconds of reperfusion just at the beginning of 24 hours of reperfusion. Then blood and liver samples were collected to measure serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and liver oxidative stress parameters including superoxide dismutase (SOD) activity and malondialdehyde (MDA) level. Renal IR caused a significant increase in liver functional indices as demonstrated by increased serum AST and ALT compared to sham group. These parameters reduced significantly in POC group compared to IR group. Liver MDA levels increased and SOD activity decreased in IR group compared to sham group. Induction of POC reduced the elevated liver MDA levels and increased the reduced liver SOD activity. These results revealed that renal IR injury causes liver damage as a remote organ and POC protects liver from renal IR injury by a modification in the hepatic oxidative stress status.

Ischemic Postconditioning Assessment in the Liver of Rats Undergoing Mesenteric Ischemia and Reperfusion

“…Seifi et al [14] evaluated the protective effect of IPC on liver damage after kidney I/R. Rats underwent renal ischemia for 45 minutes and IPC was carried out in four cycles of I/R, each with a 10-second duration.…”

Possible Protective Effect of Bone Marrow-Mesenchymal Stem Cells (BM-MSCs) Against the Remote Liver Injury Induced by Renal Ischemia Reperfusion in Male Albino Rats

“…hepatocytes, Von-kupffer cells, extra) in response to injury [36]. recruitment of neutrophils, activates T cells, and induces expression of other cytokines and chemokines such as TNF-α and IL-6 in liver tissue [11,37]. Moreover, other studies showed that following experimental renal IRI in knockout mice for TNF-α or neutralized with TNF-α antibodies displayed reduced hepatic injury after renal IRI [1].…”

“…The increasing mortality rate in cases with acute renal injury necessitates designing strategies to assess the effect of renal injury on distant organs [11]. Therefore, several studies [8,[1][2][3][4][5][6][7][8][9][10][11][12][13][14] tried to protect liver from remote injury induced by renal IRI for the prevention and attenuation of acute renal injury related morbidity.…”

Potential Hepatic Protection by Erythropoietin and Ischemic Conditioning in a Rat Model of Renal Ischemia-Reperfusion Injury

“…Further studies showed that harmful effects of renal I/R are not limited to the kidney, but extend to other organs including liver [6] , lung [7] , brain [8] , heart [9] and gut [10] leading to what is called remote organ injury (ROI), in a process of organ crosstalk by which AKI can lead to multiple organ dysfunction or even failure [10,11] .…”

“…Humoral and/or cellular factors are thought to be the cause of hepatic injury secondary to I/R. Previous studies have shown that acute kidney injury causes an increase in leukocytic infiltration and induces oxidative stress in the liver resulting in hepatic dysfunction [6,13,14] .…”