类表皮生长因子域7促进颅脑损伤模型大鼠脑微循环的修复与重建.

BACKGROUND: Vascular endothelial cell damage is shown to be closely related to blood brain barrier function disorder after traumatic brain injury. Epidermal growth factor-like domain 7 (EGFL7) is an important factor to promote angiogenesis. Whether EGFL7 can promote traumatic brain injury repair by activating angiogenesis remains unknown. OBJECTIVE: To explore the mechanisms by which EGFL7 promotes angiogenesis after traumatic brain injury in rats. METHODS: Forty-two healthy adult male rats were randomly divided into craniocerebral injury group (n=36, craniocerebral injury model was established by impacting rat dura mater with modified Feeney method) and sham group (n=6, only complete dura mater was exposed) and the rats were divided into six subgroups according to the sample time after injury: 1 hour, 6 hours, 24 hours, 3 days, 7 days and 14 days, 6 rats in each subgroup. The contusion lesion and the surrounding brain tissue were obtained after the neurological injury score was available. Another 18 rats were selected and randomized into three groups (n=6/group) to establish craniocerebral injury model. rAd-vector, rAd-EGFL7 and combined PI3K/Akt pathway inhibitor rAd-EGFL7+LY294002 was respectively injected into the ventricles of rats at 1 hour after injury. Samples were obtained at 12 hours later. RESULTS AND CONCLUSION: (1) RT-PCR, western blot assay and immumohistochemical staining results showed that the EGFL7 and CD34 were significantly up-regulated in rat brain after craniocerebral injury (P < 0.05). The expression of EGFL7 peaked on day 3 (P < 0.05), and the expression of CD34 had the same trend with EGFL7. The number of angiogenesis peaked on day 7. (2) After 12 hours of the rAd-EGFL7 microinjection in rat brain at 1 hour post-injury, the expression levels of EGFL7, CD34, pAkt and cyclin D1 were significantly up-regulated and the F0X01 expression was significantly down-regulated (all P < 0.05). (3) Microinjection of rAd-EGFL7 and PI3K/Akt inhibitor in rat brain at 1 hour post-injury, the EGFL7 expression was not significantly changed, but the CD34 expression was significantly inhibited (P < 0.05), and the number of angiogenesis was significantly decreased (P < 0.05). (4) To conclude, up-regulated EGFL7 in the injured brain tissue may be related to angiogenesis after traumatic brain injury. Overexpression of the EGFL7 promotes the angiogenesis in the injured brain tissue through activating PI3K/Akt signaling. [ABSTRACT FROM AUTHOR]