Brain inflammation induced by ischemic stroke is an important cause of secondary brain
injury. The nuclear factor kappa B (NF-κB), mitogen-activated protein kinase (MAPK), and …

Cerebral ischemia/reperfusion injury is the main cause of neurological deficit following
stroke. Pleckstrin homology-like domain, family A, member 1 (PHLDA1) is increasingly …

Inflammatory reaction after ischemia-reperfusion contributes significantly to a worsened
prognosis, and microglia activation is the main resource of inflammation in the nervous …

Background Galectin-3 acts as a mediator of microglial inflammatory response following
stroke injury. However, it remains unclear whether inhibiting galectin-3 protects against …

Background Inflammatory response triggered by innate immunity plays a pivotal element in
the progress of ischemic stroke. Receptor-interacting kinase 2 (RIP2) is implicated in …

Background and purpose Ischemic stroke activates Toll-like receptors (TLRs), triggering
rapid inflammatory cytokine production. Axl signaling has multiple roles, including regulating …

The crosstalk between astrocytes and microglia plays a pivotal role in neuroinflammation
following ischemic stroke, and phenotypic distribution of these cells can change with the …

Rationale: It is known that neuroinflammation plays a critical and detrimental role in the
development of cerebral ischemia/reperfusion (I/R), but the regulation of the cyclic GMP …

Cerebral stroke is one of the leading causes of death and permanent disability worldwide.
Toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB) p65 play a critical role in …

Microglial polarization mediated neuroinflammation plays an important role in the
pathological process of stroke. The aim of this study is to determine whether baicalein …