摘要
目的探讨胃促生长素(Ghrelin)在创伤性脑损伤(traumatic brain injury,TBI)小鼠中的神经保护作用。方法通过电子脑皮质撞击仪(eCCI)构建C57BI76小鼠TBI模型。24只小鼠按照随机数字表法分为假手术(Sham)组、TBI组.Ghrelin干预组(Ghrelin组),每组8只。Sham组仅开骨窗但不进行撞击损伤,TBI组和Ghrelin组小鼠建立TBI模型.Ghrelin组小鼠分别于伤前和伤后1 h腹腔注射Ghrelin各0.5 g/kg,Sham组和TBI组小鼠均注射等量生理盐水。采用激光散斑血流成像系统实时监测脑血流灌注量变化,运动诱发电位观察神经电生理改变,以及改良神经功能缺陷评分(mNSS)评价神经功能缺损状况。结果TBI组小鼠与Sham组相比血流灌注量明显降低(t=-12.36,P<0.01),创伤对侧下肢运动诱发电位潜伏期延长、波幅降低(t=5.03,-11.55,均P<0.01),神经功能缺陷评分显著升高(t=9.34,P<0.01).然而与TBI组比较,Ghrelin组小鼠TBI后12 h血流灌注量显著增加[(196.87±17.36)PU/mm2,(123.62+8.04)PU/mm2,t=10.45,P<0.01],运动诱发电位潜伏期缩短[(5.30±0.33)ms,(6.80±0.97)ms,t=-5.01,P<0.01],波幅升高[(2.21±0.16)mV,(1.27+0.27)mV,t=9.65,P<0.01],TB I后24 h神经功能缺陷评分明显降低[(4.9±1.2)分,(8.44±2,6)分,t=-3.87,P<0.01]。结论Ghrelin可通过增加TBI小鼠脑血流灌注量,降低神经功能缺损程度,以及促进运动功能恢孚以发挥显著的神经保护作用。
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<O.01),longer latency and lower amplitude of motor evoked potential(MEP)(≪=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,PvO.01),while the latency of MEP decreased((5.30±0.33)ms vs(6.80±0.97)ms,t=-5.01,Pv0.01),the amplitude of MEP increased((2.21±0.16)mV vs(1.27±0.27)mV,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土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.
作者
邵雪非
朱雷
衣泰龙
李博
程世翔
Shao Xuefei;Zhu Lei;Yi Tailong;Li Bo;Cheng Shixiang(Department of Neurosurgery,Yijishan Hospital of Wannan Medical College,Wuhu 241001,China;Tianjin Key Laboratory of Neurotrauma Repair,Institute of Traumatic Brain Injury and Neuroscience of Chinese People's Armed Police Force(PAP},Characteristic Medical Center of PAP,Tianjin 300162,China)
出处
《中华行为医学与脑科学杂志》
CAS
CSCD
北大核心
2019年第11期978-982,共5页
Chinese Journal of Behavioral Medicine and Brain Science
基金
国家自然科学基金项目(81891003)
安徽省高校自然科学研究重大项目(KJ2018ZD027)
天津市临床医学研究中心科技重大专项(15ZXLCSY00040)
全军技术产品研究项目(AWS15J001)。
