Post-stroke depression (PSD), a frequent and disabling complication of stroke, has a strong impact on almost thirty percent of stroke survivors. The pathogenesis of PSD is not completely clear so far. Neuroinflammation following stroke is one of underlying mechanisms that involves in the pathophysiology of PSD and plays an important function in the development of depression and is regarded as a sign of depression. During the neuroinflammation after ischemic stroke onset, both astrocytes and microglia undergo a series of morphological and functional changes and play pro-inflammatory or anti-inflammatory effect in the pathological process of stroke. Importantly, astrocytes and microglia exert dual roles in the pathological process of PSD due to the phenotypic transformation. We summarize the latest evidence of neuroinflammation involving in PSD in this review, focus on the phenotypic transformation of microglia and astrocytes following ischemic stroke and reveal the dual roles of both microglia and astrocytes in the PSD via modulating the neuroinflammation.

Ischemic stroke is one of the most cases worldwide, with high rate of morbidity and mortality. In the pathological process of ischemic stroke, neuroinflammation is an essential process that defines the functional prognosis. After stroke onset, microglia, astrocytes and the infiltrating immune cells contribute to a complicated neuroinflammation cascade and play the complicated roles in the pathophysiological variations of ischemic stroke. Both microglia and astrocytes undergo both morphological and functional changes, thereby deeply participate in the neuronal inflammation via releasing pro-inflammatory or anti-inflammatory factors. Flavonoids are plant-specific secondary metabolites and can protect against cerebral ischemia injury via modulating the inflammatory responses. For instances, quercetin can inhibit the expression and release of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, IL-6 and IL-1β, in the cerebral nervous system (CNS). Apigenin and rutin can promote the polarization of microglia to anti-inflammatory genotype and then inhibit neuroinflammation. In this review, we focused on the dual roles of activated microglia and reactive astrocyte in the neuroinflammation following ischemic stroke and discussed the anti-neuroinflammation of some flavonoids. Importantly, we aimed to reveal the new strategies for alleviating the cerebral ischemic stroke.

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.

Cerebral ischemic injury is one of the main causes of adult disability and death. Although significant progress has been made, cerebral ischemia continues to be a major risk to public health worldwide. The Rho kinase (ROCK) signaling pathway has been reported to be significantly involved in many mechanisms of cerebral injury. Although ROCK is ubiquitously expressed in all tissues, ROCK2 subtype expression in brain and the spinal cord is more abundant and improves with age. This makes it a promising target for new therapeutic approaches. In this article, we review the current knowledge on the involvement of ROCK in cerebral ischemia injury and neurodegenerative changes after cerebral injury. After a detailed description of the mechanism of ROCK involvement in axonal regeneration and synaptic function, different roles of ROCK1 and ROCK2 in neurons under physiological and pathological conditions are compared and discussed. In addition, different functions of genetic and pharmacological inhibitions of ROCK1 and ROCK2 on cerebral injury are discussed.