2-APB (2-Aminoethyl Diphenylborinate)

2-APB, an inositol 1, 4, 5-trisphosphate receptor (IP₃R) inhibitor, obviously attenuates the intracellular Ca²⁺ release and cardiomyocyte apoptosis induced by oxygen and glucose deprivation (OGD) stimulation and EndoA2 knockdown.^[3]

Neonatal Sprague-Dawley rats (1 to 3 days old) are exposed to hypothermia until they became unresponsive and are then euthanized by cervical dislocation. Primary culture of NRCMs is performed. The cells are seeded at a density of 5 x 10⁶ cells/ml in Dulbecco's modified Eagle's medium supplemented with 10% fetal bovine serum and 0.1 mM 5-bromodeoxyuridine. After 24 h, NRCMs are subjected to various treatments as described below. To assess the effects of EndoA2 on cardiac injury, the cells are transfected with EndoA2 siRNA or Ad-EndoA2. After transfection for 36 h, the cells are stimulated with oxygen and glucose deprivation (OGD) for another 12 h. Incubation of sodium phenylbutyrate (4-PBA), Cyclosporin A (CsA), 1,2-bis(o-aminophenoxy)ethane-N,N,N ,N -tetraacetic acid (BAPTA) or 2-Aminoethoxydiphenylborate (2-APB) is 2 h before OGD stimulation.Cardiomyocytes are cultured in serum-free, glucose and sodium pyruvate-free DMEM at 37 ℃ in an anoxia chamber saturated with 94% N₂/5% CO₂/ 1% O₂.

2-APB increases the basilar artery (BA) wall thickness and reduced the BA lumen diameter, inducing significant vascular changes, also alleviates cell apoptosis at 24 hours after SAH.^[4]