Gallic acid treatment protects intestinal tissue against ischaemia-reperfusion.

BACKGROUND: This study aimed to investigate the protective effects of gallic acid (GA) in the rat intestine against ischaemia-reperfusion (IR) injury. MATERIALS AND METHODS: Thirty male Wistar albino rats with a mean weight of 200-250 g were used. Animals were categorized into the sham, IR, and IR+GA groups. Ischaemia of the intestine was induced for 3 h by occluding the superior mesenteric artery (SMA) and then left for 3 h of reperfusion. In the IR+GA group, after ischaemia induction, 50 mg/kg GA was orally administered to the animals. Blood samples were collected for biochemical assays. Intestinal tissues were excised for histopathologic and immunohistochemical processing. RESULTS: Malondialdehyde (MDA) levels were increased, and catalase (CAT) and glutathione (GSH) levels were decreased in the IR group compared to the sham group. After GA treatment, MDA levels decreased and CAT and GSH levels increased in the GA-treated group compared to the IR group. In the sham group, normal intestinal histology was observed. In the IR group, the villi structures were completely degenerated. In the IR+GA group, histology was improved after GA treatment. In the sham group, the caspase-3 reaction was generally negative in the epithelium and glands. In the IR group, the caspase-3 reaction increased in apoptotic bodies and inflammatory cells. The caspase-3 reaction was negative in goblet cells and the epithelium. A moderate caspase-3 reaction was observed in the IR+GA group. The beclin-1 reaction was negative in epithelial cells and goblet cells in villi in the sham group. In the IR group, the beclin-1 reaction was positive in the degenerated villi. An intense beclin-1 reaction was also observed in some inflammatory cells. After GA treatment, the beclin-1 reaction was positive in a few cells. In general, moderate beclin-1 positivity was observed. CONCLUSIONS: Gallic acid, with its antioxidative effect, inhibited the apoptotic pathway (caspase-3) through beclin-1 regulation.

Daidzein alleviated the pathologies in intestinal tissue against ischemia-reperfusion.

OBJECTIVE: The aim of this study was to investigate the effect of daidzein against intestinal ischemia-reperfusion injury in rats. MATERIALS AND METHODS: Thirty male Wistar albino rats with a mean weight of 200-250 gr were used. Animals were categorized into sham, ischemia-reperfusion (IR), and IR+Daidzein group. 3-hour ischemia of intestine was created by occluding superior mesenteric artery and then left for 3-hour reperfusion. In IR+daidzein group, after ischemia, 50 mg/kg daidzein was orally administered to the animals. Blood samples were collected for biochemical assays. Intestine tissues were excised for histopathologic and immunohistochemical processing. RESULTS: Malondialdehyde (MDA) increased, and Catalase (CAT) and Glutathione (GSH) decreased after IR in intestine tissue. Daidzein treatment decreased MDA and increased CAT and GSH level in IR+Daidzein group. Histopathologically, sham group showed normal intestinal tissue histology. In IR group, epithelial and villi degeneration, edema, leukocyte infiltration, vascular dilatation and congestion was observed. After Daidzein treatment, these pathologies were improved. The caspase-6 expression was mainly negative in sham group. After IR, caspase-6 reaction was very high in IR group. Daidzein reduced caspase-6 expression in IR+Daidzein group. Ki67 immune staining was negative in the sham group. In IR group, Ki67 expression was increased in inflammatory cells, deep glandular cells and in some goblet cell nuclei. In IR+Daidzein group, Ki67 expression was decreased due to reduced inflammation. CONCLUSIONS: IR injury causes oxidative stress, apoptosis and inflammation. Daidzein treatment improved histopathology against intestinal IR.

Effect of ellagic acid on damage caused by hepatic ischemia reperfusion in rats.

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.