中华创伤杂志
中華創傷雜誌
중화창상잡지
Chinese Journal of Traumatology
2010年
1期
13-15
,共3页
王天懿%朱玉群%栾伟华%王燕斌%杨昭徐
王天懿%硃玉群%欒偉華%王燕斌%楊昭徐
왕천의%주옥군%란위화%왕연빈%양소서
细胞凋亡%氧化性应激%脑损伤%肝损伤
細胞凋亡%氧化性應激%腦損傷%肝損傷
세포조망%양화성응격%뇌손상%간손상
Apoptosis%Oxidative stress%Brain injuries%Liver injuries
目的 探讨细胞凋亡和氧化应激在大鼠创伤性脑损伤(TBI)后应激性肝损伤中的作用.方法 改良Allen法建立TBI模型.40只雄性Wistar大鼠按随机数字表法分为5组:正常对照组、TBI后6,12,24,48 h组.测定血清肝酶、肝组织超氧化物歧化酶(SOD)和丙二醛,流式细胞仪检测肝细胞凋亡率.光镜及电镜观察肝组织学变化.结果 TBI后血清ALIT和AST显著进行性升高,肝组织SOD减少,丙二醛增加;TBI早期即6 h,电镜下可见凋亡细胞,细胞凋亡率显著增加且达峰值;病理显示TBI后肝组织进行性损伤.结论 TBI后出现应激性肝损伤,细胞凋亡和氧化应激可能参与其发病过程.
目的 探討細胞凋亡和氧化應激在大鼠創傷性腦損傷(TBI)後應激性肝損傷中的作用.方法 改良Allen法建立TBI模型.40隻雄性Wistar大鼠按隨機數字錶法分為5組:正常對照組、TBI後6,12,24,48 h組.測定血清肝酶、肝組織超氧化物歧化酶(SOD)和丙二醛,流式細胞儀檢測肝細胞凋亡率.光鏡及電鏡觀察肝組織學變化.結果 TBI後血清ALIT和AST顯著進行性升高,肝組織SOD減少,丙二醛增加;TBI早期即6 h,電鏡下可見凋亡細胞,細胞凋亡率顯著增加且達峰值;病理顯示TBI後肝組織進行性損傷.結論 TBI後齣現應激性肝損傷,細胞凋亡和氧化應激可能參與其髮病過程.
목적 탐토세포조망화양화응격재대서창상성뇌손상(TBI)후응격성간손상중적작용.방법 개량Allen법건립TBI모형.40지웅성Wistar대서안수궤수자표법분위5조:정상대조조、TBI후6,12,24,48 h조.측정혈청간매、간조직초양화물기화매(SOD)화병이철,류식세포의검측간세포조망솔.광경급전경관찰간조직학변화.결과 TBI후혈청ALIT화AST현저진행성승고,간조직SOD감소,병이철증가;TBI조기즉6 h,전경하가견조망세포,세포조망솔현저증가차체봉치;병리현시TBI후간조직진행성손상.결론 TBI후출현응격성간손상,세포조망화양화응격가능삼여기발병과정.
Objective To explore the effect of cell apoptosis and oxidative stress on stressive liv-er injury after traumatic brain injury (TBI) in rats. Methods The model of TBI was duplicated by u-sing modified Allen's mehtods. Forty male Wistar rats were randomly divided into control group and groups at 6,12,24,48 hours after TBI. The serum levels of ALT and AST as well as the levels of superox-ide dismutase (SOD) and malandialdehyde in liver tissue were measured. The index of hepatocyte apopto-sis was detected through flow cytometer. Pathological changes of liver tissues were observed under light and electron microscopes. Results After TBI, the serum levels of ALT and AST were significantly in-creased, while malondialdehyde was increased and SOD decreased in liver tissues. The electron micro-scope showed that the index of hepatocyte apoptosis reached a peak at 6 hours after TBi. Aggressive inju-ries of the liver tissues were observed after TBI, showed by pathological observations. Conclusion Cell apoptosis and oxidative stress may be involved in the pathogenesis of stressive liver injury after TBI.