Alteration of renal functional, oxidative stress and inflammatory indices following hepatic ischemia-reperfusion

Abstract

Liver ischemia/reperfusion (IR) injury is a complex phenomenon that may cause local as well as remote organ injuries. Reactive oxygen species (ROS) along with many pro- and anti- inflammatory cytokines are implicated in the development of organ injury. The renal functional, histological, oxidative stress and inflammatory indices were studied during a short and a longer period of liver IR. Rats were subjected to either sham operation or 90 min partial liver ischemia followed by 4 or 24 h of reperfusion. Serum ALT, AST, ALK and LDH levels, BUN and creatinine, renal MDA level, SOD and catalase activities were evaluated as well as serum IL-6 and IL-10 concentrations along with renal histological evaluation. Ninety minutes liver ischemia /4 h reperfusion caused an increase in BUN and renal MDA levels and a decrease in SOD and catalase activities. It also caused an increase in serum IL-6 and IL-10 levels. 24 h liver reperfusion resulted in a reduction in BUN levels and lower oxidative damages demonstrated by a decrease in renal MDA levels and an increase in renal SOD and catalase activities comparing to 4 h reperfusion group. Evaluations indicated improvement in histology such as less cytoplasmic vacuolation and lower tubular debris. Serum inflammatory indices (IL-6 and IL-10 levels) were also reduced. This study showed that liver IR damage causes renal injury including functional, inflammatory and oxidative status changes. The remote kidney damage was then improved by continuing reperfusion from 4 to 24 h.

Propofol alleviates liver oxidative stress via activating Nrf2 pathway

“…Among the various ROS, OH and O2 À are the most frequently investigated free radicals. MDA, an end product of lipid peroxidation, has been investigated in many reports and used to indicate the presence and the extent of oxidative damage [7,31,32] It has been reported that highly effective antioxidant systems counteract oxidative injury processes at all levels including prevention of the formation of ROS, detoxification, and repair of oxidative damage [33]. Nrf2, a transcription factor, acts as the central controller of expression of many antioxidant enzymes [10] involved in direct scavenging of ROS [11].…”

Protective effect of magnesium on renal function in STZ-induced diabetic rats

“…Increasing BUN and plasma creatinine, has been reported as waste products of metabolism following kidney injury and they has known biomarkers of kidney degeneration [43]. In this study, the elevation of plasma BUN with hyperglycemia can be proposed as indicator for renal dysfunction [44].…”

Global Consequences of Liver Ischemia/Reperfusion Injury

“…Systemic inflammatory response may induce renal injury [20, 25]. Circulating levels of proinflammatory cytokines and transcription factors, including interleukin (IL)-6, tumor necrosis factor-alpha (TNF- α ), and high mobility group box (HMGB) 1, are increased and their release from the liver may promote inflammatory changes in the kidney after liver ischemia/reperfusion [25–28]. Kupffer cells activation plays the predominant role in the production and release of these cytokines.…”

“…Activated neutrophils [33] aggregate in the subendothelial space, where they release reactive oxygen species (ROS), enzymes, and cytokines, causing direct renal injury [36] and the recruitment of monocytes and macrophages leading to further aggravation of the oxidative injury. Kadkhodaee et al reported that liver ischemia/reperfusion causes renal injury including oxidative status changes as shown by the increase in renal malondyaldehyde (MDA) levels and the decrease in superoxide dismutase (SOD) and catalase activity [28]. Similar results were reported in other studies showing that hepatic ischemia and reperfusion may cause oxidative stress to renal tissue and that administration of antioxidants seems to have a beneficial effect via the glutathione (GSH) system and the modulation of MDA levels [37, 38].…”