BCL2 and transient ischemic attack: Because of the importance and sensitivity of CA1 area of hippocampus and the pathophysiological mechanisms of cerebral ischemia, this study provided the novel therapeutic window of nesfatin-1 by the inhibition of astrocytes activation as an inflammatory response, increased the expression of the antiapoptotic protein Bcl-2, and also decrease in Bax-mediated neuronal cell apoptosis after transient cerebral ischemia in rats; however, further experiments are required to clarify these beliefs.