Neuroprotective effects of Ghrelin on traumatic brain injury in mice / 中华行为医学与脑科学杂志

ABSTRACT

Objective@#To investigate the neuroprotective effect of Ghrelin on traumatic brain injury (TBI) in mice.@*Methods@#TBI model of C57BL / 6 mice was established by electronic cortical impact instrument (eCCI). According to the random figure table method, twenty-four mice were randomly divided into sham group(Sham group), TBI group and Ghrelin intervention group(Ghrelin group) with 8 mice in each group. The model of TBI was established in TBI group and Ghrelin group.The mice in Ghrelin group was injected intraperitoneally 0.5 g/kg before and 1 h after injury respectively. And the mice Sham group and TBI group were injected with the same amount of normal saline. The changes of cerebral blood perfusion (CBP) were monitored in real time by laser speckle contrast analysis(LSCI), the changes of neuroelectrophysiology were observed by monitoring motor evoked potential (MEP), and the status of neurological deficit was evaluated by modified neurological deficit score (mNSS).@*Results@#Compared with Sham group, the mice in TBI group had significantly lower cerebral blood perfusion(CBP) (t=-12.36, P<0.01), longer latency and lower amplitude of motor evoked potential (MEP) (t=5.03, -11.55, all P<0.01), and significantly higher mNSS scores (t=9.34, P<0.01). However, compared with the TBI group, the cerebral blood perfusion(CBP) of Ghrelin group increased significantly at 12 h after TBI((196.87±17.36) PU/mm2 vs (123.62±8.04)PU/mm2, t=10.45, P<0.01), while the latency of MEP decreased((5.30±0.33)ms vs (6.80±0.97)ms, t=-5.01, P<0.01), the amplitude of MEP increased((2.21±0.16)mV vs (1.27±0.27)mV, t=9.65, P<0.01). And compared with the TBI group, the neurological deficit score of Ghrelin group decreased significantly at 24 h after TBI((4.9±1.2) vs (8.4±2.6), t=-3.87, P<0.01).@*Conclusion@#Ghrelin exhibits a significant neuroprotective role by increasing cerebral blood flow perfusion, reducing the degree of neurological deficit and promoting motor function recovery in TBI mice.