Batatasin-III protects cerebral vascular endothelium by regulating mitochondrial function and production of nitric oxide

This study assessed the effect of batatasin-III on cerebral microvascular endothelial cell (EC) injury. Endothelial cell injury was induced in isolated cells by oxygenglucose deprivation/reperfusion (OGD/R) conditions. During 4 h of OGD insult, cells were treated with batatasin-III at different concentrations, and an MTT assay was performed to estimate cellular viability. Nitric oxide, mitochondrial membrane potential (MMP), and release of lactate dehydrogenase (LDH) were determined in ECs exposed to OGD/R. Cerebral ischemia was performed to induce brain injury to assesses the effect of batatasin-III. There was improvement in the viability of cell and reduction of release of LDH in batatasin-III-treated, OGD/R-induced EC injury. Treatment with batatasin-III ameliorates the altered integrity of mitochondrial membrane and expression of apoptotic proteins in OGD/R injured ECs. Apoptosis of neuronal cells and infarct size were reduced in batatasin-III-treated middle cerebral artery occlusion (MCAO) rats, and pathological changes were reversed. Based on study data, we concluded that cerebral injury was attenuated by batatasin-III treatment by reducing oxidative stress and cellular apoptosis.