Establishment and study of a new mouse brain blast injury model
10.3760/cma.j.issn.1671-0282.2019.01.009
- VernacularTitle:新型小鼠脑爆震伤模型的建立及研究
- Author:
Changci TONG
1
;
Yunen LIU
;
Yubiao ZHANG
;
Peifang CONG
;
Lin SHI
;
Xiuyun SHI
;
Ying LIU
;
Mingxiao HOU
;
Hongxu JIN
Author Information
1. 北部战区总医院急诊医学部
- Keywords:
Brain blast injury;
Simulation device;
Spatial memory learning ability;
Blood-brain barrier;
Injury
- From:
Chinese Journal of Emergency Medicine
2019;28(1):44-49
- CountryChina
- Language:Chinese
-
Abstract:
Objective To develop a new type of blast injury simulator to establish a mouse model of brain blast injury and study its damage mechanism. Methods Thirty healthy Kunming mice were randomly(random number) divided into the normal control group and brain blast injury model (TBI) group. A mouse model of traumatic brain injury was prepared by a self-developed explosive injury simulator. Morris water maze, Evans blue experiment and HE staining were used to observe the effects of shockwave exposure on spatial memory, blood-brain barrier, and pathological changes of brain tissues. T test was used for statistical analysis. Western blot method was used for detecting expression of brain injury markers Tau, S100β, Choline, inflammatory factors IL-1β, IL-4, IL-6, IL-10, NF-κB, apoptosis factors Bcl-2, Bax, Caspase3, and oxide protein stress-related factors IREα, MDA5, COX2 SOD1, and SOD2. Results Compared with the normal control group, (11.2±2.1) s, the time of searching platform in the TBI group was (54.6±8.4) s, was significantly longer (t=-19.330, P<0.05), and the EB exudation in the TBI group was 3.22 times (t=-13.903, P<0.05). Pathological staining revealed neuronal damage in the hippocampus, and TBI induced brain injury markers Tau(0.26±0.03 vs 0.46±0.04,t=-9.788, P<0.05), S100β(0.54±0.03 vs 0.74±0.02,t=-12.433, P<0.05) and Choline(0.54±0.05 vs 0.80±0.04, t=-7.970, P<0.05), inflammatory cytokines IL-1β(0.22±0.04 vs 0.31±0.05,t=-3.431, P<0.05), IL-4(0.65±0.02 vs 0.97±0.03, t=-18.927, P<0.05), IL-6(0.88±0.05 vs 1.07±0.08, t=-9.488, P<0.05) and NF-κB(0.80±0.06 vs 1.03±0.07,t=-4.507, P<0.05), and pro-apoptotic cytokines Bax(0.66±0.04 vs 0.78±0.04, t=-13.007, P<0.05) and Caspase3(0.44±0.03 vs 0.60±0.05, t=-4.472, P<0.05), oxidative stress-related factor pro IREα(0.72±0.06 vs 1.07±0.04, t=-9.665, P<0.05), MDA5(0.47±0.02 vs 0.77±0.02, t=-23.678, P<0.05) and expression of COX2(0.70±0.07 vs 0.86±0.02, t=-6.421, P<0.05), inhibition of inflammation inhibitory factor IL-10(1.14±0.06 vs 0.74±0.07, t=13.729, P<0.05), inhibition of apoptosis factors Bcl-2(0.72±0.05 vs 0.46±0.02, t=11.491, P<0.05) and inhibition of oxidative stress factors SOD1(1.17±0.05 vs 0.99±0.01, t=7.731, P<0.05) and SOD2(0.81±0.05 vs 0.61±0.04, t=10.257, P<0.05) expression. Conclusions The brain injury induced by blast exposure can induce spatial learning and memory loss, blood brain barrier disruption, neuronal damage hippocampus in mice, and promote the expression of brain injury markers, induce inflammation, oxidative stress and apoptosis. The self-developed explosive shock simulator successfully establishes a mouse brain blast injury model.
