Table 1.
Type of Stroke | Experimental Model | Findings | References |
---|---|---|---|
NHIBI | Carotid ligation mouse model | MCs associated genes upregulated | [70] |
Carotid ligation rat model | Rapid increase of activated MCs in the brain | [71,72] | |
MCs pharmacological inhibition reduced MCs migration, brain damage and glial activation | |||
Transient focal ischemia rat model | Rapid increase of activated MCs and histamine in the brain | [73] | |
Ibotenate mouse model | IL-9 exacerbated brain damage by activating MCs | [74] | |
MCs pharmacological inhibition reduced brain damage | |||
Ischemic Stroke | OGD mouse MCs | OGD promoted MCs activation | [83,84,85] |
OGD mouse MCs and neurons | OGD-activated MCs induced neurotoxicity | [83] | |
MCs pharmacological inhibition reduced MCs-induced neurotoxicity | |||
MCAO mouse model | MCs associated gene upregulated | [87] | |
MC-deficient mice showed decreased BBB leakage, brain edema and neutrophils infiltration | [90] | ||
MCs pharmacological inhibition decreased BBB leakage, brain edema and neutrophils infiltration | |||
Meningeal MCs worsen infiltration of granulocytes and macrophages, brain swelling, and infarct size | [93] | ||
Four-vessel occlusion rat model | Modulation of MCs number and histamine levels | [88] | |
MCAO rat model | MCs pharmacological activation increased edema formation | [89] | |
MCs pharmacological inhibition decreased brain swelling, BBB leakage and neutrophils infiltration | |||
MC-deficient rats showed decreased brain swelling, BBB leakage, and neutrophils infiltration | |||
MCAO rat model | Increased MCs gelatinase activity | [91] | |
MCs pharmacological activation increased gelatinase activity | |||
MCs pharmacological inhibition decreased gelatinase activity | |||
MC-deficient rats displayed decreased gelatinase activity | |||
MCAO rat model treated with rtPA | MCs pharmacological inhibition reduced rtPA-induced hemorrhagic conversion, brain swelling, and neutrophil infiltration. | [98] | |
MC-deficient rats displayed decreased rtPA-induced hemorrhagic conversion, brain swelling, and neutrophil infiltration. | |||
Patients | Lack of MCs in penumbra brain region | [94] | |
ICH | Blood infusion rat model | MCs pharmacological activation increased brain damage. | [106] |
MCs pharmacological inhibition decreased brain damage, improved neurologic outcome | |||
MC-deficient rats displayed decreased brain damage, improved neurologic outcome | |||
Collagenase infusion mouse model | MCs activation | [107,108] | |
MCs pharmacological inhibition decreased brain damage, improved neurologic outcome | |||
Collagenase infusion rat model treated with rtPA | MCs pharmacological inhibition reduced rtPA-induced hematoma growth, hemispheric expansion, mortality, and neurologic deficits. | [109] | |
SAH | CA rat model | MCs in aneurysm wall | [119] |
MCs pharmacological inhibition reduced inflammation and CA size and thinning | |||
Co-culture rat MCs and smooth muscle cells | Histamine and thromboxane inhibitors decreased MCs-mediated vasoconstriction | [119] | |
Patients | MCs in aneurysm wall | [120,121,122] | |
MCs in the muscular layer of cerebral arteries | [123] |
BBB: blood brain barrier; CA: cerebral aneurysm; ICH: intracerebral hemorrhage; MCAO: middle cerebral artery occlusion; MCs: mast cells; NHIBI: neonatal hypoxic-ischemic brain injury; OGD: oxygen and glucose deprivation; rtPA: recombinant tissue plasminogen activator; SAH: subarachnoid hemorrhage.