Cortical benign fibromatous tumor (fibroma) of the kidney.

OBJECTIVE

Ischemia (I) causes lack of oxygen delivery to the tissues, leading to hypoxia and cellular damage. Reperfusion (R) is the re-blooded of the tissue; however, it may cause more tissue damage than ischemia alone in some cases. During IR, number of free radicals and metabolic by-products increases. To prevent this, cellular antioxidant system is activated but it may not be enough to restore the cellular activities. The aim of this study was to investigate the potential protective effect of Ellagic Acid on damage caused by hepatic IR in rats.

MATERIALS AND

METHODS

Thirty rats were divided into three groups: (1) Sham group - no drug administration but only midline laparotomy was performed in the abdomen; (2) Ischemia-Reperfusion (IR) group - ischemia was applied for 1 hour by sealing the portal vein and hepatic artery, then vessels were reperfused for 6 hours; (3) IR+Elagic Acid (EA) group - after IR, 10 mg/kg of EA was given intraperitonially to the rats once a day for 28 days. Oxidative stress markers were analyzed by blood collection. Hepatic tissues were processed for histological and immunohistochemical analysis.

RESULTS

MDA level and MPO activity were increased and GSH content was decreased after IR group was compared to sham group. After EA treatment, these values were improved in IR+EA group. IR caused hepatocyte degeneration, sinusoidal dilatation, leukocyte infiltration and disintegrity of hepatic tissue. EA administration improved histopathology after IR. IR injury increased TNF-α and Caspase-9 expression in hepatocytes and vascular endothelial cells in IR group; however, both decreased in EA-received group.

CONCLUSIONS

Ellagic Acid may reduce oxidative stress level and prevent induction of inflammation and cell death against hepatic IR.