OBJECTIVE  To study the effect of Gei Herba extract LBZ-55 on motor function injury after cerebral ischemia in mice induced by photothrombosis, and to explore its potential mechanism.

METHODS  The model of focal acute cerebral ischemia was established by photothrombosis model in mice. LBZ-55 was administered intragastrically for 14 d after operation. The motor function of mice was evaluated by cylinder and grid experiments every other day, and the volume of cerebral infarction was detected by toluidine blue staining; the changes of cerebral blood flow were monitored by laser speckle imaging, and the number of blood vessels around the infarct was detected by immunohistochemistry on the 7th day after operation; the leakage of blood-brain barrier was detected by Evans blue staining; oxygen glucose deprivation was used to simulate cerebral ischemia in vitro, and the migration ability and tube formation ability of bEnd.3 cells were detected.

RESULTS  LBZ-55 administration for 14 consecutive days after PT modeling significantly reduced the step-out rate and asymmetry index, but did not reduce the volume of cerebral infarction on the ischemic side, suggesting that LBZ-55 improved neurological damage in mice with cerebral ischemia, and its effect may not be related to direct neuroprotective effects; continuous administration of LBZ-55 for 7 days significantly increased the cerebral blood flow of the affected side of the mice, the vascular density around the infarcted brain tissue, and the expression of VEGFA protein in the infarcted and surrounding cortex. The leakage of blood-brain barrier was reduced, and the expression of claudin-5 and ZO-1 protein was significantly increased. LBZ-55 could promote the migration ability of cells after oxygen-glucose deprivation, and the number and branches of tubules formed were significantly increased.

CONCLUSION  LBZ-55 can improve the neurological function of mice after cerebral ischemia induced by photothrombosis, improve the cerebral blood flow in ischemic area and the density of surrounding blood vessels, significantly increase the expression of VEGFA protein in ischemic brain tissue, and reduce the damage of blood-brain barrier. This effect may be related to the mechanism of promoting angiogenesis after cerebral ischemia.