Effects Of Butylphthalide On Endogenous Neural Stem Cells Proliferation In Mice With Cerebral Ischemia And Reperfusion

Ischemic cerebral vascular disease is a kind of neurological disease with highmortality and mutilation. The high incidence of this disease presents with the ageincreasing. There is still no very effective and satisfying therapy in clinical practice.Thus, to develop a new effective and feasible therapy is an important content ofneurological research.In this study, focal cerebral ischemia and reperfusion was induced in mice withthe intraluminal suture method, and then the mice were treated with NBP. Theproliferating cells were labeled with BrdU (5-bromodeoxyuridine), and an 18-scorescale was performed to evaluate the neurological deficits. The proliferation ofendogenous NSCs in dentate gyrus of hippocampus in ipsilateral cerebral hemispherewas observed on the 3rd, 7th, 11th and 21st day after cerebral ischemia. The influenceof NBP on neurological function recovery was observed. The pattern of NSCsproliferation in mice after cerebral ischemia, and whether NBP can enhance the NSCsproliferation were elucidated.Results: (1)Groups treated with NBP got higher neurological scores in mice,especially on the 7th day and 11th day after cerebral ischemia and reperfusion,Whereas there was no difference between the low-dose group and the high-dosegroup. (2) In contrast to normal and sham-operated group, the number ofBrdU-labeled cells in DG of ipsilateral hippocampus began to increase on the 3rd dayafter cerebral ischemia and reperfusion, increased obviously on the 7th and 11th dayafter ischemia, and reached its peak on the 11th day after ischemia, then the number ofBrdU-labeled cells fell on the 21st day after ischemia, when the BrdU-labeled cellsbegan to migrate to GCL. (3) There is no significant difference among the numbers ofBrdU-labeled cells of the groups treated with or without NBP. Conclusions: (1) NBP can improve neurological function recovery in miceafter cerebral ischemia and reperfusion to a certain extent, especially on the 7th and11th day after ischemia. (2) Endogenous neural stem cells in DG of mice canproliferate in response to cerebral ischemia, and the proliferating state reaches a peakon the 11th day after ischemia, and then falls down. About 3 weeks after ischemia,NSCs may migrate from SGZ to GCL, where they may differentiate into neurons. (3)There is no evidence that NBP can enhance the proliferation of endogenous NSCs inDG of mice after cerebral ischemia.