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Antineuroinflammatory effects of dl-3-n-butylphthalide conferred by stimulation of Foxp3 and Ki-67 in an ischemic stroke model


 Background

Dl-3-n-butylphthalide (NBP) has been widely used for the treatment of ischemic stroke in China. However, its mechanisms of action have not been fully elucidated.
Methods

We established a permanent middle cerebral artery occlusion (pMCAO) rat model and administered 4 mg/kg/d NBP by tail vein injection for 9 days. Changes in some molecules related to neuroinflammation, neovascularization and nerve regeneration were observed, such as MALDI-TOF MSI to study the distribution of phospholipids in the brain, LA-ICP MSI to observe the changes of Foxp3, Ki-67 and pCREB, immunohistochemistry to investigate NLRP3 and its downstream inflammatory products Caspase-1 and IL-1β.
Results

These results showed that NBP attenuated ischemic damage in pMCAO rats, accompanied by improving neurological deficits. It was revealed for the first time in an animal stroke model that NBP decreased the levels of PE (18:0), NLRP3, Caspase-1 and IL-1β, while increasing the levels of several phospholipids, such as PA (16:0/18:1), PA (18:0/22:6), PE (16:0/22:6), PE (P-18:0/22:6), PE (18:0/22:6), PS (18:0/22:6), PI (18:0/20:4), Foxp3, Ki-67 and pCREB, in the ischemic brain region.
Conclusion

These results provide evidence that NBP can reduce neuroinflammation in brain tissue and promote the regeneration of nerves and blood vessels, thus exerting a protective effect on neuromorphology and function.