摘要
目的:探讨氧化应激(OS)在大鼠创伤性脑损伤(TBI)后应激性肝损害(HSI)中的作用.方法:用改良Allen法建立TBI模型.40只健康Wister大鼠随机分为5组,正常对照组、颅脑致伤后6、12、24、48h时相组.酶学法检测血清ATL和AST水平,ABC-ELISA法测定血清TNF-α水平.硫代巴比妥酸法测定MDA水平变化,化学发光法测定SOD水平变化.光镜及电镜下观察肝脏组织学改变.结果:颅脑致伤后12h,各组血ALT和AST、TNF-α水平及肝组织MDA明显增加,肝组织SOD显著减少,与对照组比较差异均显著(252.92±56.29vs41.17±7.88;283.12±45.28vs45.22±6.57;1138.27±212.02vs210.56±28.22;15.21±0.36vs6.14±0.25;78.13±3.12vs135.58±5.58,P<0.01或0.05);TBI各组光镜和电镜可观察到肝组织不同程度受损.结论:TBI后早期可出现HSI,OS可能参与了其发病过程.
AIM： To explore the effect of oxidative stress （OS） on hepatic stress injury （HSI） secondary to traumatic brain injury （TBI）. METHODS： The animal model was established using an improved Allen＇s method. Forty healthy male Wistar rats had been divided randomly into five groups： control group and 6, 12, 24 and 48 h TBI posttraumatic groups. The serum levels of ALT and AST were measured using enzymic assay. The serum tumor necrosis factor-α （TNF-α） was detected using ABC-ELISA technique. The MDA values of liver tissue were measured with thiobarbituric acid method, and SOD of liver tissue was measured using chemiluminescence. And pathological changes of liver tissue were observed under light and electronic microscopy. RESULTS： At early period of HSI, the serum levels of ALT, AST and TNF-α and the MOD values of liver tissue were markedly increased in all TBI groups, and the SOD values of liver tissue were significantly decreased compared with control group （252.92 ± 56.29 vs 41.17 ± 7.88; 283.12 ± 45.28 vs 45.22 ± 6.57; 1138.27 ± 212.02 vs 210.56 ± 28.22; 15.21 ± 0.36 vs 6.14 ± 0.25; 78.13 ± 3.12 vs 135.58 ± 5.58, P 〈 0.01 or 0.05）. Liver tissue injuries at varied degrees were observed under light and electron microscopy in each TBI group. CONCLUSION： Oxidative stress may be involved in the pathogenesis of HSI which occurs early secondary to traumatic brain injury.
出处
《世界华人消化杂志》
CAS
北大核心
2008年第30期3433-3436,共4页
World Chinese Journal of Digestology
