摘要目的 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.

abstractsObjective 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.