BCL2 and intracerebral hemorrhage: Moreover, this hormone was able to decrease inflammation and neuronal apoptosis after intracerebral hemorrhage by increasing the expression of integrin αVβ5 (irisin receptor), p-AMPK (promotes microglial/macrophage polarization to the M2-phenotype), and Bcl-2, while IL-1β, TNF-α, myeloperoxidase (MPO), and BAX expression were lowered after intracerebral hemorrhage in the mouse model [66].