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Effects of seawater immersion on open traumatic brain injury in rabbit model.
Brain Research ( IF 2.7 ) Pub Date : 2020-05-20 , DOI: 10.1016/j.brainres.2020.146903
Kai-Li Liu 1 , Xiao-Jing Yu 1 , Tian-Ze Sun 2 , Yi-Chang Wang 3 , Meng-Xuan Chen 4 , Yan-Wen Su 5 , Hao-Chen Zhang 6 , Yan-Mei Chen 1 , Hong-Li Gao 1 , Xiao-Lian Shi 7 , Jie Qi 1 , Ying Li 1 , Hong-Bao Li 1 , Wei-Jiang Dong 2 , Jian-Kang He 5 , Yu-Ming Kang 1
Affiliation  

We emulated instances of open traumatic brain injuries (TBI) happened in a maritime disaster. New Zealand rabbit animal models were used to evaluate the pathophysiological changes in open TBI with and without the influence of artificial seawater. New Zealand rabbits were randomly divided into 3 groups. Control group consisted of only normal animals. Animals in TBI and TBI+Seawater groups underwent craniotomy with dura mater incised and brain tissue exposed to free-fall impact. Afterward, only TBI+Seawater group received on-site artificial seawater infusion. Brain water content (BWC) and permeability of blood-brain barrier (BBB) were assessed. Reactive oxygen species levels were measured. Western blotting, immunofluorescence were employed to detect: apoptosis-related factors Caspase-3, Bax and Bcl-2; angiogenesis-related factors CD31 and CD34; astrogliosis-related factor glial fibrillary acidic protein (GFAP); potential neuron injury indicator neuron-specific enolase (NSE). Hematoxylin & eosin, Masson-trichrome and Nissl stainings were performed for pathological observations. Comparing to Control group, TBI caused abnormal neurons shape; increased BWC; compromised BBB integrity; increased ROS, Bax, CD31, CD34, Caspase-3 and GFAP expressions; decreased Bcl-2 and NSE expression. Seawater immersion caused all changes, except BWC, to become more significant. Seawater immersion worsens the damage inflicted to brain tissue by open TBI. It aggravates hypoxia in brain tissue, upregulates ROS expression, increases neuron sensibility to apoptosis-inducing factors, and promotes angiogenesis as well as astrogliosis.

中文翻译:

海水浸泡对兔模型开放性颅脑损伤的影响。

我们模拟了海上灾难中发生的开放性脑外伤 (TBI) 实例。新西兰兔动物模型用于评估开放性TBI在人工海水影响和不影响下的病理生理变化。新西兰兔随机分为3组。对照组仅由正常动物组成。TBI 和 TBI+海水组中的动物接受了硬脑膜切开和脑组织暴露于自由落体冲击的开颅手术。之后,只有TBI+海水组接受了现场人工海水输注。评估脑含水量(BWC)和血脑屏障(BBB)的通透性。测量活性氧物质水平。采用Western blotting、免疫荧光法检测:凋亡相关因子Caspase-3、Bax、Bcl-2;血管生成相关因子 CD31 和 CD34;星形胶质细胞增生相关因子胶质纤维酸性蛋白 (GFAP); 潜在神经元损伤指标神经元特异性烯醇化酶 (NSE)。进行苏木精和伊红、马松三色和尼氏染色以进行病理观察。与对照组相比,TBI 导致神经元形状异常;增加 BWC;BBB 完整性受损;增加 ROS、Bax、CD31、CD34、Caspase-3 和 GFAP 的表达;Bcl-2 和 NSE 表达降低。海水浸泡导致除 BWC 之外的所有变化变得更加显着。海水浸泡会加重开放性 TBI 对脑组织造成的损伤。它加重脑组织缺氧,上调ROS表达,增加神经元对凋亡诱导因子的敏感性,促进血管生成和星形胶质细胞增生。潜在神经元损伤指标神经元特异性烯醇化酶 (NSE)。进行苏木精和伊红、马松三色和尼氏染色以进行病理观察。与对照组相比,TBI 导致神经元形状异常;增加 BWC;BBB 完整性受损;增加 ROS、Bax、CD31、CD34、Caspase-3 和 GFAP 的表达;Bcl-2 和 NSE 表达降低。海水浸泡导致除 BWC 之外的所有变化变得更加显着。海水浸泡会加重开放性 TBI 对脑组织造成的损伤。它加重脑组织缺氧,上调ROS表达,增加神经元对凋亡诱导因子的敏感性,促进血管生成和星形胶质细胞增生。潜在神经元损伤指标神经元特异性烯醇化酶 (NSE)。进行苏木精和伊红、马松三色和尼氏染色以进行病理观察。与对照组相比,TBI 导致神经元形状异常;增加 BWC;BBB 完整性受损;增加 ROS、Bax、CD31、CD34、Caspase-3 和 GFAP 的表达;Bcl-2 和 NSE 表达降低。海水浸泡导致除 BWC 之外的所有变化变得更加显着。海水浸泡会加重开放性 TBI 对脑组织造成的损伤。它加重脑组织缺氧,上调ROS表达,增加神经元对凋亡诱导因子的敏感性,促进血管生成和星形胶质细胞增生。进行马森三色和尼氏染色以进行病理观察。与对照组相比,TBI 导致神经元形状异常;增加 BWC;BBB 完整性受损;增加 ROS、Bax、CD31、CD34、Caspase-3 和 GFAP 的表达;Bcl-2 和 NSE 表达降低。海水浸泡导致除 BWC 之外的所有变化变得更加显着。海水浸泡会加重开放性 TBI 对脑组织造成的损伤。它加重脑组织缺氧,上调ROS表达,增加神经元对凋亡诱导因子的敏感性,促进血管生成和星形胶质细胞增生。进行马森三色和尼氏染色以进行病理观察。与对照组相比,TBI 导致神经元形状异常;增加 BWC;BBB 完整性受损;增加 ROS、Bax、CD31、CD34、Caspase-3 和 GFAP 的表达;Bcl-2 和 NSE 表达降低。海水浸泡导致除 BWC 之外的所有变化变得更加显着。海水浸泡会加重开放性 TBI 对脑组织造成的损伤。它加重脑组织缺氧,上调ROS表达,增加神经元对凋亡诱导因子的敏感性,促进血管生成和星形胶质细胞增生。海水浸泡导致除 BWC 之外的所有变化变得更加显着。海水浸泡会加重开放性 TBI 对脑组织造成的损伤。它加重脑组织缺氧,上调ROS表达,增加神经元对凋亡诱导因子的敏感性,促进血管生成和星形胶质细胞增生。海水浸泡导致除 BWC 之外的所有变化变得更加显着。海水浸泡会加重开放性 TBI 对脑组织造成的损伤。它加重脑组织缺氧,上调ROS表达,增加神经元对凋亡诱导因子的敏感性,促进血管生成和星形胶质细胞增生。
更新日期:2020-05-20
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