中华创伤杂志
中華創傷雜誌
중화창상잡지
Chinese Journal of Traumatology
2009年
8期
739-742
,共4页
邓哲%杨欣建%赵中江%周泽强%刘德红%谢玉刚%孙冀武%姚彬%郑晓英
鄧哲%楊訢建%趙中江%週澤彊%劉德紅%謝玉剛%孫冀武%姚彬%鄭曉英
산철%양흔건%조중강%주택강%류덕홍%사옥강%손기무%요빈%정효영
甘氨酸%休克%创伤性%肝损伤%热休克蛋白70%肿瘤坏死因子-α
甘氨痠%休剋%創傷性%肝損傷%熱休剋蛋白70%腫瘤壞死因子-α
감안산%휴극%창상성%간손상%열휴극단백70%종류배사인자-α
Glycine%Shock,traumatic%laver injury%Heat-shock protein 70%Tumor necrosis factor-α
目的 研究甘氨酸对大鼠创伤性休克后肝组织热休克蛋白70(HSP70)和TNF-αmRNA表达的影响,探讨其对大鼠创伤性休克继发肝损伤的可能保护机制.方法 建立创伤性休克动物模型,120只Wistar大鼠按随机数字表法分成3组:创伤性休克组(休克组)、甘氨酸治疗组(治疗组)和对照组.在复苏开始时,治疗组大鼠将甘氨酸按100 mg/kg溶于0.5 ml等渗盐水后经颈静脉输入,休克组输以同体积的等渗盐水.分别于复苏后3,6,12,24及48 h 5个时相点处死大鼠.采用RT-PCR法检测肝组织HSP70和TNF-α mRNA表达;观察肝组织病理改变并测定血清ALT和AST水平. 结果 休克组复苏后3 h肝组织HSPTO和TNF-αmRNA表达即增加,复苏后6 h达高峰,治疗组肝组织HSP70 mRNA表达于复苏后12 h达高峰.与休克组比较,治疗组各时相点肝组织TNF-α mRNA表达明显降低(P<0.05),HSP70 mRNA表达明显增强(P<0.05),血清ALT和AST明显降低(P<0.05),肝组织光镜下病理损害明显改善(P<0.05). 结论甘氨酸可能通过增强肝组织HSP70 mRNA表达及抑制TNF-α mRNA表达的途径降低创伤性休克后继发肝损伤的程度.
目的 研究甘氨痠對大鼠創傷性休剋後肝組織熱休剋蛋白70(HSP70)和TNF-αmRNA錶達的影響,探討其對大鼠創傷性休剋繼髮肝損傷的可能保護機製.方法 建立創傷性休剋動物模型,120隻Wistar大鼠按隨機數字錶法分成3組:創傷性休剋組(休剋組)、甘氨痠治療組(治療組)和對照組.在複囌開始時,治療組大鼠將甘氨痠按100 mg/kg溶于0.5 ml等滲鹽水後經頸靜脈輸入,休剋組輸以同體積的等滲鹽水.分彆于複囌後3,6,12,24及48 h 5箇時相點處死大鼠.採用RT-PCR法檢測肝組織HSP70和TNF-α mRNA錶達;觀察肝組織病理改變併測定血清ALT和AST水平. 結果 休剋組複囌後3 h肝組織HSPTO和TNF-αmRNA錶達即增加,複囌後6 h達高峰,治療組肝組織HSP70 mRNA錶達于複囌後12 h達高峰.與休剋組比較,治療組各時相點肝組織TNF-α mRNA錶達明顯降低(P<0.05),HSP70 mRNA錶達明顯增彊(P<0.05),血清ALT和AST明顯降低(P<0.05),肝組織光鏡下病理損害明顯改善(P<0.05). 結論甘氨痠可能通過增彊肝組織HSP70 mRNA錶達及抑製TNF-α mRNA錶達的途徑降低創傷性休剋後繼髮肝損傷的程度.
목적 연구감안산대대서창상성휴극후간조직열휴극단백70(HSP70)화TNF-αmRNA표체적영향,탐토기대대서창상성휴극계발간손상적가능보호궤제.방법 건립창상성휴극동물모형,120지Wistar대서안수궤수자표법분성3조:창상성휴극조(휴극조)、감안산치료조(치료조)화대조조.재복소개시시,치료조대서장감안산안100 mg/kg용우0.5 ml등삼염수후경경정맥수입,휴극조수이동체적적등삼염수.분별우복소후3,6,12,24급48 h 5개시상점처사대서.채용RT-PCR법검측간조직HSP70화TNF-α mRNA표체;관찰간조직병리개변병측정혈청ALT화AST수평. 결과 휴극조복소후3 h간조직HSPTO화TNF-αmRNA표체즉증가,복소후6 h체고봉,치료조간조직HSP70 mRNA표체우복소후12 h체고봉.여휴극조비교,치료조각시상점간조직TNF-α mRNA표체명현강저(P<0.05),HSP70 mRNA표체명현증강(P<0.05),혈청ALT화AST명현강저(P<0.05),간조직광경하병리손해명현개선(P<0.05). 결론감안산가능통과증강간조직HSP70 mRNA표체급억제TNF-α mRNA표체적도경강저창상성휴극후계발간손상적정도.
Objective To investigate the effects of glycine on the expression of HSP70 and TNF-α mRNA in the liver tissue of rats with traumatic shock and explore the protective mechanism of glycine a-gainst secondary liver injury after traumatic shock. Methods The traumatic shock model was established and 120 Wistar rats were divided randomly into three groups: treatment group, shock group and control group. At the beginning of resuscitation, the rats in the treatment were injected with 0.5 ml isotonic saline containing 100 mg/kg glycine, those rats in the shock group were injected only with 0.5 ml isotonic saline. The rats in three groups were killed at 3, 6, 12, 24 and 48 hours after resuscitation respectively. The ex-pression of HSP70 and TNF-α mRNA in the liver tissue were detected by RT-PCR, pathological changes were observed and serum ALT and AST were measured. Results The expressions of HSP70 and TNF-α mRNA in the liver tissue of rats in the shock group began to increase at 3 hours and both reached the peak value at 6 hours after resuscitation, but the expression of HSP70 mRNA in the treatment group reached the peak value at 12 hours after resuscitation. Compared with the control group, the expression of HSP70 mR-NA in the treatment group increased significantly and that of TNF-α mRNA decreased siganicantly, serum ALT and AST decreased and pathological damage was relieved significantly (all P < 0.05). Conclusion By enhancing the expression of HSP70 mRNA and decreasing the expression of TNF-α mRNA, glycine may play a protective role against the secondary damage of liver after traumatic shock.