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

Figure 4

Mechanism of the anti-inflammatory effects of ischemic postconditioning (IPO). Ischemic postconditioning places stress on the cell, triggering endogenous protective mechanisms. Immunosuppression is reduced by decreasing peripheral humoral immunity. Intracellular: ischemic postconditioning places stress on the cell, triggering endogenous protective mechanisms. Reduction of mitochondrial cytochrome C results in immunosuppression, which leads to a decrease in the levels of inflammatory cytokines and chemokines. IL-1β: interleukin 1 beta; TNF-α: tumor necrosis factor alpha; TLR-2: toll-like receptor 2; TLR-4: toll-like receptor 4; Cyto C: cytochrome C; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells.