Conclusions
Our results showed that HPC significantly promotes neurogenesis after MCAO and ameliorates neuronal injury.
Methods
SD rats were used to establish the MCAO model. Nissl staining and Golgi staining were used to confirm the neuronal injury status in the MCAO model. Immunofluorescence, transmission electron microscopy, Western blot, and qPCR were used to observe the effects of HPC on neurogenesis. At the same time, the hypothesis that HPC could affect proliferation, apoptosis, differentiation, and migration of NSC was verified in vitro.
Results
Hypoxic preconditioning significantly ameliorated the neuronal injury induced by MCAO. Compared with MCAO group, the dendrites, Edu+ /SOX2+ , Edu+ /DCX+ , Edu+ /NeuN+ , Edu+ /GFAP+ , and Edu+ /Tubulin+ positive cells in the HPC + MCAO group exhibited significantly difference. Similarly, axonal and other neuronal injuries in the HPC + MCAO group were also ameliorated. In the in vitro experiments, mild HPC significantly enhanced the viability of NSCs, promoted the migration of differentiated cells, and reduced apoptosis. Conclusions: Our results showed that HPC significantly promotes neurogenesis after MCAO and ameliorates neuronal injury.