Search

Background Acute mesenteric ischemia is a life-threatening clinical entity. 2-Aminoethoxydiphenyl borate (2-APB) is a membrane-permeable modulator of intracellular inositol triphosphate-induced calcium release. We investigated the effects of different 2-APB doses on intestinal ischemia-reperfusion injury in an experimental rat model. Methods We divided 24 Wistar albino rats into four groups: sham, control, ischemia-reperfusion +2 mg/kg 2-APB, and ischemia-reperfusion +4 mg/kg 2-APB. The sham group only underwent laparotomy for 1 h 30 min. A 30-min period of mesenteric ischemia was induced in the control and two treatment groups, followed by 1 h of reperfusion. Before the laparotomy, 2 mg/kg and 4 mg/kg 2-APB was administered i.v. in the treatments groups, and blood samples were collected after reperfusion. Serum levels of malondialdehyde, superoxide dismutase, glutathione, total antioxidant capacity, tumor necrosis factor (TNF)-alpha, and interleukin-6 were analyzed. Intestinal tissues were taken for histopathological, DNA fragmentation, and terminal deoxynucleotidyl transferase dUTP nick end labeling analyses to determine the proportion of apoptotic cells. Results 2-APB reduced serum malondialdehyde, TNF-alpha, and interleukin-6 levels. However, superoxide dismutase and total antioxidant capacity levels increased significantly in the 4-mg/kg 2-APB group (p < 0.05). The intestinal histopathological injury scores were significantly higher in the control group; these injuries were prevented in the 4-mg/kg 2-APB dose group. DNA damage after ischemia-perfusion decreased significantly in the 4-mg/kg 2-APB group compared with the control group. Conclusion 2-APB decreases oxidative stress and cell injury. Administering 4 mg/kg 2-APB prevented ischemia-perfusion injury by diminishing histological damage.

Background: To investigate the protective effect of 2-aminoethyl diphenylborinate (2-APB) against ischemia-reperfusion (I/R) injury in the rat kidney by an experimental study. Materials and methods: Thirty male Sprague-Dawley rats were randomly divided into the following three groups: (1) sham group, (2) I/R group, and (3) I/R + 2-APB group. Renal I/ R injury was induced by clamping the left renal pedicle for 45 min after right nephrectomy, followed by 3 h of reperfusion. The therapeutic agent 2-APB was administered intravenously at a dose of 2 mg/kg 10 min before renal ischemia. Glutathione, superoxide dismutase, total antioxidant capacity, malondialdehyde, tumor necrosis factor a, interleukin 6, aspartate aminotransferase, alanine aminotransferase, and creatinine levels were measured from blood samples, and the rats were sacrificed subsequently. Tissue samples were scored histopathologically. Visualization of apoptotic cells was performed using the terminal deoxynucleotidyl transferase dUTP nick end labeling staining method. Results: 2-APB significantly reduced serum malondialdehyde, tumor necrosis factor a, interleukin 6, aspartate aminotransferase, alanine aminotransferase, and creatinine levels in the I/R injury group. However, glutathione, superoxide dismutase, and total antioxidant capacity levels increased significantly. Histopathologic scores were significantly better and the rate of apoptosis was lower in the 2-APB group. Conclusions: 2-APB reduces oxidative stress and damage caused by renal I/R injury. The results of this study demonstrate that 2-APB can be used as an effective agent against I/R injury in the kidney.