Batatasin-III Regulates the NO Production and Mitochondrial Membrane Potential in Cerebral Vascular Endothelial Injury: <i>in-vivo</i> and <i>in-vitro</i> Study

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Microvascular endothelial cell injury causes cerebral injury. Present study evaluates the protective effect of batatasin-III against cerebral microvascular endothelial cell (EC) injury by in-vivo and in-vitro study. Endothelial cells were isolated from rats and exposed to oxygenglucose deprivation/reperfusion (OGD/R) condition to induced endothelial injury cell. These cells were treated with batatasin-III (5, 10 and 20 μM) during the 4h period of OGD insult and cells were further incubated for 24 h under the normal condition. Cell viability was estimated by MTT assay and LDH release, mitochondrial membrane potential and level of NO was estimated in (OGD/R) exposed ECs. Apoptosis of ECs was estimated by Hoechst 33258 and expression of apoptotic protein by western blot assay in ECs. Moreover in vivo study was performed to determine the effect of batatasin-III on cerebral ischemia induced brain injured rats. Result of investigation reveals that treatment with batatasin-III ameliorates the cell viability and percentage of LDH release in the OGD/R induced EC injury. Expression of apoptotic protein and integrity of mitochondrial membrane was alleviated in batatasin-III treated (OGD/R) induced EC injury. Level of NO and apoptosis of ECs was reduced in batatasin-III treated group than OGD/R group of ECs. Moreover, infract size, apoptosis of neuronal cells and pathological changes were ameliorated in batatasin-III treated group than MCAO group of rats. In conclusion, data reveals that batatasin-III treatment reduces the cellular apoptosis by reduces the oxidative stress and improving mitochondrial membrane potential in microvascular endothelial cell injury and improved the cerebral injury.