“…However, under pathological stress, the secretion of cerebral astrocytes and microglia increases, thus IL-6 expression increases (2,3,19,20), which mediates a series of pathophysiological reactions. Such IL-6-induced pathophysiological reactions include: (i) Changes in cerebral microcirculation, resulting in increases in vascular permeability and damage to the BBB, thus promoting the formation and progression of cerebral edema; (ii) increases in leukocyte adhesion and endothelial cells, promoting extravascular infiltration and activation of inflammatory cells (4,19); (iii) increases in the proliferation and reparation of cerebral glial cells in damaged brain regions (5,22); (iv) induction of complications associated with TBI, as well as multiple organ failure, for example, increases in IL-6 have a negative muscle strength effect and cytotoxic effect, which causes damage to the structure and function of the left ventricle, promoting deterioration of patient cardiac function and hemodynamics (7,8,23,24); and (v) problems associated with fever and local metabolism, affecting patient prognosis and rehabilitation. As an inflammatory cytokine, IL-6 expression has been found to increase significantly in the CNS following TBI and the levels of IL-6 in the CSF has been negatively correlated with Glasgow Coma Scale and Glasgow Outcome Scale scores following injury (9,25).…”