Effects of 2-Aminoethyl Diphenylborinate, a Modulator of Transient Receptor Potential and Orai Channels in Subarachnoid Hemorrhage: An Experimental Study

Abstract Cerebral vasospasm remains to be a serious problem that affects morbidity and mortality in patients with Subarachnoid Hemorrhage (SAH) during neurosurgery. Our study aims to demonstrate the role of the transient receptor potential channel, and other channels, for Ca 2+ in the etiology of cerebral vasospasm by using 2-Aminoethyl diphenylborinate (2-APB), and to determine the effective dose range of a previously unstudied pharmacological agent which can limit vasospasm. An experimental study was performed using 32 Sprague-Dawley rats divided into 4 groups: Group 1 (Sham, n=8), Group 2 (SAH group, blood drawn from the right femoral artery was injected into the cisterna magna, n=8), Group 3 (2-APB group, SAH rats intraperitoneally administered with 0.5 mg/kg 2-APB, n=8), and Group 4 (2-APB-2 group, SAH rats intraperitoneally administered with 2 mg/kg 2-APB, n=8). Rats were sacrificed after 24 hours and SOD, GPx, MDA, TNF-α, and IL-1β in the brain tissue and serum were measured. In the histopathological investigation of brain tissue, luminal diameter and wall thickness of basilar artery (BA) were measured, and apoptotic cells in the hippocampus were counted after caspase staining. Autologous arterial blood injection into the cisterna magna caused vasospasm in rats. 2-APB treatment, which increased BA wall thickness and reduced BA lumen diameter, induced significant vascular changes. In addition, 2-APB alleviated cell apoptosis at 24 h after SAH.2-APB treatment, which increased BA wall thickness and reduced BA lumen diameter, induced significant vascular changes.