Overview of Experimental and Clinical Findings regarding the Neuroprotective Effects of Cerebral Ischemic Postconditioning

Figure 5

Mechanism of antiapoptotic effects of ischemic postconditioning (IPO). ER stress is closely related to the function of mitochondria. Ischemic postconditioning places stress on the cell, triggering endogenous protective mechanisms that reduce ER stress and protect the mitochondria. This attenuates apoptosis in the CNS. P-eif2α: phosphoeukaryotic initiation factor 2 alpha; GRP78: glucose-regulated protein 78; CHOP: C/EBP homologous protein; ER: endoplasmic reticulum; Bim: Bcl-2-like protein; Bcl-2: B-cell lymphoma 2; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells; JNK: c-Jun N-terminal kinase; pAKT: phosphorylated protein kinase B; ERK: extracellular signal-related kinase; Bad: Bcl-2-associated death promoter; mitokATP: mitochondrial ATP-sensitive potassium channels; Cyto C: cytochrome C.