Progress in understanding role of inflammation in pathogenesis of post-ischemia cerebral injury

Many mechanisms are involved in the pathogenesis of cerebral ischemia injury. Inflammation is an important part of post-ischemic injury. This important pathological process exists in each stage. Microglia and astrocytes are activated in the acute stage of ischemia and produce inflammatory factors such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α. Inflammatory factors act on endothelial cells, neutrophils, and lymphocytes to produce more inflammatory factors, which in turn induce apoptosis, aggravate calcium overload, promote the release of toxic amino acids, and result in the production of free radicals via the TLR4/NF-κB and PI3K/Akt signal pathways. Inflammation cascade causes irreversible neurological damage in the subacute phase. With the activation of macrophages and the transformation of morphology and function of microglia, the body changes from the state of injury to the state of protection. At the same time, some pro-inflammatory factors such as TNF-α and IL-6 exhibit neuroprotective effects. And the factors such as TGF-β1 and IGF-1, which promote the proliferation and repair of nerve cells, increase and promote the repair process. The inflammatory response after cerebral ischemic injury is different in all stages. This paper reviews the progress in understanding the role of inflammation in the pathogenesis of post-ischemia cerebral injury. Key words: Inflammation; Cerebral infarction; Chemokines