The role of RhoA/ROCK pathway in the ischemic stroke-induced neuroinflammation

It is widely known that ischemic stroke is the prominent cause of death and disability. To date, neuroinflammation following ischemic stroke represents a complex event, which is an essential process and affects the prognosis of both experimental stroke animals and stroke patients. Intense neuroinflammation occurring during the acute phase of stroke contributes to neuronal injury, BBB breakdown, and worse neurological outcomes. Inhibition of neuroinflammation may be a promising target in the development of new therapeutic strategies. RhoA is a small GTPase protein that activates a downstream effector, ROCK. The up-regulation of RhoA/ROCK pathway possesses important roles in promoting the neuroinflammation and mediating brain injury. In addition, nuclear factor-kappa B (NF-κB) is another vital regulator of ischemic stroke-induced neuroinflammation through regulating the functions of microglial cells and astrocytes. After stroke onset, the microglial cells and astrocytes are activated and undergo the morphological and functional changes, thereby deeply participate in a complicated neuroinflammation cascade. In this review, we focused on the relationship among RhoA/ROCK pathway, NF-κB and glial cells in the neuroinflammation following ischemic stroke to reveal new strategies for preventing the intense neuroinflammation.