Table 3.

Therapeutic goals and related mechanisms of drugs in ischemic stroke.

Drugs	Mechanisms	Polarization pathway	Therapeutic effects	Clinical aspects
Minocycline	Inhibiting nuclear translocation of NF-KB, regulates STAT1/STAT6 pathway	Reduces the production of M1 and enhances the expression of M2	Inhibiting the activation and activation of microglia, the production of reactive oxygen species and cell apoptosis	Reducing the brain water content and brain edema, improve functional recovery in ischemic stroke
Metformin	Inhibits the inflammatory pathway mediated by brain NF-κB	M2	Reduces infarct volume and improves neurological deficits, promoting tissue repair	Chronic post-stroke therapy
rosiglitazone	Unknown	Promotes polarization of microglia toward the M2 phenotype	Educing oxidative stress, attenuating excitotoxicity	Improve white matter integrity after stroke, contributing to stroke long-term recovery
Dexmedetomidine	Unknown	Unknown	Diminish neuroinflammation in the mouse brain	Neuroprotective effect
Etifoxine	Unknown	Unknown	Reduce leukocyte infiltration, control the production of pro-inflammatory cells in microglia, improve the integrity of the blood-brain barrier	Reduce neurological deficits and infarct volume, limit brain inflammation, and provide protection against ischemia/reperfusion injury