Effect of 2-Aminoethoxydiphenyl Borate on Acute Cerebral Ischemia-Reperfusion Injury: An Experimental Study

Objective In cerebral ischemia-reperfusion (I/R) injury, an increase in intracellular calcium concentration is the leading factor in cell death. The store-operated Ca2+ entry (SOCE) is responsible for Ca2+ entry into the cell and takes place mediated by the Orai1, Stromal-interacting molecule1 (STIM1), and Stromal-interacting molecule2 (STIM2) proteins. 2-Aminoethoxydiphenyl Borate (2APB) is a chemical agent that prevents store-operated Ca2+ entry into the cell. In this study, it was investigated the possible protective effect of 2-APB on the occurred injury in the experimental cerebral I/R model in rats. Materials and Methods In the study, eighteen male rats were divided into three groups (n=6). In the Sham group, only surgical procedure was applied without cerebral I/R model. Ischemia-reperfusion model was created for rats in the cerebral I/R and cerebral I/R-2APB groups. Reperfusion was realized one-hour later. Ten-minutes before reperfusion, 2-APB was administered to the rats in the cerebral I/R-2APB group. After three hours of reperfusion, the rats were sacrificed and their brains were removed. The changes that occurred in the brain tissues were investigated by using histochemical methods, the TUNEL, and immunohistochemical staining. Results In the cerebral I/R group, it was determined that the histological structure was impaired and apoptosis and expression of Orai1, STIM1, and STIM2 proteins were increased compared to the sham group. In the 2-APB administrated group, it was revealed that the tissue damage and apoptotic cells were decreased, and Orai1, STIM1, and STIM2 expression were significantly inhibited. Conclusion As a result, it has been demonstrated that 2-APB may be effective in decreasing apoptosis and neuronal damage by reducing SOCE-mediated Ca2+ influx into the cell in cerebral I/R damaged tissue.