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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.
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ObjectiveToestablisharatmodelofincreasedbloodflow-inducedpulmonaryarterialhypertension generatedbyanastomosisoftheleftcommoncarotidarterytoleftexternaljugularvein.Methods 45maleSDratswere divided into three groups:the shunt group , the ligation group and the sham group .At twelve weeks after the procedure , the general status of the rats was observed . Heart conditions , cardiac output and shunt patency were measured by echocardiography .Right ventricular systolic pressure ( RVSP ) and Qp/Qs were checked by catheterization . Right ventricular hypertrophy index ( RVHI) was calculated and lung tissues were examined by pathology using hematoxylin -eosin and elastin Van Gieson staining .All data were analyzed statistically by one-way ANOVA test using SPSS 16.0.Results There was no significant difference in body weight gains between the groups .The patency rate of shunt was 84.6%.The heart was enlarged in the group shunt .Cardiac output increased significantly in the shunt group than that in the other two groups [(309.8 ±33.1) mL/min?kg vs.(245.6 ±31.9) mL/min?kg, (240.8 ±30.9)mL/min?kg, respectively, P<0.05].In the shunt group Qp/Qs was 2.16 ±0.38 and RVSP increased to (35.8 ±4.9) mmHg, RVHI was 0.3263 ± 0.0342, significantly higher than that of the other groups .The pulmonary arteriolar wall was evidently thickened in contrast to that in the sham group [ ( 22.3 ±1.7 )% vs.( 10.6 ±1.7 )%, P <0.05 ) .Conclusions Anastomosis of the left common carotid artery to left external jugular vein can successfully establish pulmonary arterial hypertension model induced by high blood flow in rats .