Delayed Energy Protection of Ischemic Preconditioning on Hepatic Ischemia/Reperfusion Injury in Rats

Abstract

Background: Hepatic ischemia/reperfusion (IR) injuries associated with hepatic resections are unresolved problems in the clinical practice. The aim of this study is to elucidate the effect of ischemic preconditioning (IPC) on the energy charge (EC) and related mechanisms at the late phase of hepatic IR injury. Methods: 30 Wistar rats were randomly divided into sham, IR and IPC groups. The model of partial hepatic IR was used. The rats were subjected to 60 min hepatic ischemia, pretreated by IPC (10/15 min) or not. After 24 h of reperfusion, serum alanine aminotransferase (ALT), nitrite/nitrate (NOx), malondialdehyde (MDA), hepatic tissue arginase activity, adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP) and EC of the liver were measured. Results: Liver injury reduced by IPC is measured by liver tissue arginase activity and serum ALT. Tissue NOx levels in rats pretreated with IPC were significantly higher than levels in the IR group (p < 0.001). Tissue levels of MDA in the liver of the IPC group were found to be significantly lower than the levels in the IR group (p < 0.001). ATP and EC levels 24 h after hepatic ischemia in rats pretreated with IPC were higher than the levels in the IR (p < 0.05). All groups had similar ADP and AMP levels in the liver tissues. The IPC procedure significantly reduced the hepatic necrosis (p < 0.001). Conclusion: The results of this study demonstrated that pretreatment with IPC improved tissue ATP, EC, and hepatic necrosis at late stages of ischemia reperfusion injury of the liver. Increased nitric oxide, reduced MDA and arginase activity seemed to play a regulatory role in this delayed protective effect of IPC.

Alpha-Lipoic Acid Protects against Hepatic Ischemia-Reperfusion Injury in Rats

“…In the present study, I/R caused significant increases in the hepatic malondialdehyde levels, end products of lipid peroxidation. This observation is in agreement with the previous studies, where elevated levels of lipid peroxidation products were increased from 40 to 80% above basal values [33][34][35] . Lipoic acid treatment abolished the increase in malondialdehyde, probably in part by scavenging the very reactive hydroxyl and peroxyl radicals.…”

Grape seed extract treatment reduces hepatic ischemia‐reperfusion injury in rats

“…In the present study, I/R caused significant increases in the hepatic malondialdehyde levels, end products of lipid peroxidation. This observation is in agreement with the previous studies, where elevated levels of lipid peroxidation products were increased from 40% to 80% above basal values (Sener et al, 2003;Ofluoglu et al, 2006;Zhu et al, 2006). Furthermore, our results demonstrated that GSE treatment abolished these increases in malondialdehyde, probably in part by scavenging the very reactive hydroxyl and peroxyl radicals.…”

“…Considerable evidence suggests that oxygen derived free radicals are involved in the hepatic injury caused by ischemia and reperfusion (Sener et al, 2003(Sener et al, , 2005Ofluoglu et al, 2006;Zhu et al, 2006). Thus, therapeutic strategies are designed to reduce free radicalinduced damage, either by intervening in the process by which free radicals are formed or by scavenging the free radicals that have already been formed.…”

Effect of Myrtus Communis L. Extracts on Attenuation of Liver Normothermic Ischemia-Reperfusion Injury

“…This observation is in agreement with the previous studies, where elevated levels of lipid peroxidation products were increased from 40% to 80 above basal values [23][24][25]. Furthermore, our results demonstrated that leaves of Myrtle Black fruit treatment can inhibit the production of oxygen radicals and prevent them from injury to liver tissue.…”