Prophylaxis with carnosol attenuates liver injury induced by intestinal ischemia/reperfusion

Abstract

AIM:To investigate the possible protective effects of carnosol on liver injury induced by intestinal ischemia reperfusion (I/R). METHODS:Rats were divided randomly into three experimental groups: sham, intestinal I/R and carnosol treatment (n = 18 each). The intestinal I/R model was established by clamping the superior mesenteric artery for 1 h. In the carnosol treatment group, surgery was performed as in the intestinal I/R group, with intraperitoneal administration of 3 mg/kg carnosol 1 h before the operation. At 2, 4 and 6 h after reperfusion, rats were killed and blood, intestine and liver tissue samples were obtained. Intestine and liver histology was investigated. Serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and interleukin (IL)-6 were measured. Liver tissue superoxide dismutase (SOD) and myeloperoxidase (MPO) activity were assayed. The liver intercellular adhesion molecule-1 (ICAM-1) and nuclear factor κB (NF-κB) were determined by immunohistochemical analysis and western blot analysis. RESULTS:Intestinal I/R induced intestine and liver injury, characterized by histological changes, as well as a significant increase in serum AST and ALT levels. The activity of SOD in the liver tissue decreased after I/R, which was enhanced by carnosol pretreatment. In addition, compared with the control group, carnosol markedly reduced liver tissue MPO activity and serum IL-6 level, which was in parallel with the decreased level of liver ICAM-1 and NF-κB expression. CONCLUSION:Our results indicate that carnosol pretreatment attenuates liver injury induced by intestinal I/R, attributable to the antioxidant effect and inhibition of the NF-κB pathway.

The Protective Effects of Curcumin on Experimental Acute Liver Lesion Induced by Intestinal Ischemia-Reperfusion through Inhibiting the Pathway of NF-κB in a Rat Model

“…We and others have reported that TNF- α and IL-6 are key mediators of liver lesion after intestinal I/R [4, 14]. In this study, the two serum cytokines increased significantly after intestinal I/R compared with the sham group ( P < 0.01, resp.).…”

Elevation of HO-1 Expression Mitigates Intestinal Ischemia-Reperfusion Injury and Restores Tight Junction Function in a Rat Liver Transplantation Model

“…The physiopathological changes in liver transplantation-induced intestinal injury include cytotoxicity and pathological changes in the intestinal mucosa barrier. Moreover, the intactness of gastrointestinal tract could have profound impact on functionality of other organs as GI has been called “motor of multiple organ failure.” Such interdependence makes liver the most vulnerable organ after intestinal injury because liver and intestine share the anatomical common pathway such as coupled vasculature [ 37 ]. Restoration of intestine barrier function through protecting the barrier structure integrity may facilitate recipients recovering from liver transplantation procedure that causes systemic changes in physiopathology.…”

Acute kidney injury in rats with or without pre‐existing chronic kidney disease: Cytokine/chemokine response

“…15,16 Together these mediators induce multiple organ failure (MOF), including acute pulmonary, hepatic and renal injury. [17][18][19][20] In this model of IIR-induced AKI, decreased renal blood flow, microvascular injury and compromised tubular function are observed within the kidneys. 19,20…”