The Effect of Etoricoxib on Hepatic Ischemia-Reperfusion Injury in Rats

Abstract

Ischemia-reperfusion (I/R) damage is known to be a pathological process which continues with the increase of oxidants and expands with the inflammatory response. There is not any study about protective effect of etoricoxib on the liver I/R damage in literature. Objective. This study investigates the effect of etoricoxib on oxidative stress induced by I/R of the rat liver. Material and Methods. Experimental animals were divided into four groups as liver I/R control (LIRC), 50 mg/kg etoricoxib + liver I/R (ETO-50), 100 mg/kg etoricoxib + liver I/R (ETO-100), and healthy group (HG). ETO-50 and ETO-100 groups were administered etoricoxib, while LIRC and HG groups were orally given distilled water by gavage. Hepatic artery was clamped for one hour to provide ischemia, and then reperfusion was provided for 6 hours. Oxidant, antioxidant, and COX-2 gene expressions were studied in the liver tissues. ALT and AST were measured. Results. Etoricoxib in 50 and 100 mg/kg doses changed the levels of oxidant/antioxidant parameters such as MDA, MPO, tGSH, GSHRd, GST, SOD, NO, and 8-OH/Gua in favour of antioxidants. Furthermore, etoricoxib prevented increase of COX-2 gene expression and ALT and AST levels. This important protective effect of etoricoxib on the rat liver I/R can be tested in the clinical setting.

Renalase as a Novel Biomarker for Evaluating the Severity of Hepatic Ischemia‐Reperfusion Injury

“…The in vivo hepatic I/R model was performed as previously described [3, 16, 17, 25]. Male C57BL/6 mice, aged 8–12 weeks, were purchased from Beijing University (Beijing, China) and maintained on a chow diet in a 12 h light/12 h dark environment at 25°C in the Animal Care Facility of Tongji Medical College.…”

“…The ischemia-reperfusion (I/R) process occurs in many clinically important events, including hepatic resectional surgery, transplantation, trauma, and hemorrhagic shock [1–3]. Hepatic I/R injury is an inevitable complication causing severe cellular death, tissues damage, and liver dysfunction, which increases the mortality [4–6].…”

The effect of nizatidine on ovarian ischaemia/reperfusion injury in rats

“…Tissue injury can lead to biochemical or structural changes (Salman et al, 2011). While histopathological methods are used to detect structural damage, biochemical damage is assessed by measuring oxidants (XO, MDA, MPO) and antioxidants (tGSH, GPO, SOD) (Kunak et al, 2015).…”

Benidipine can prevent liver ischemia reperfusion injury in rats: a biochemical and histopathological evaluation

“…This is because COX-1 is the enzyme responsible for the synthesis of cytoprotective prostaglandins, whereas COX-2 is the enzyme responsible for the synthesis of proinflammatory prostaglandins [26,27]. In the studies of Kunak et al [28], COX-2 activity was high in liver tissue with IR injury. It is not known whether the inhibitory effect of benidipine on COX-2 is direct or indirect.…”