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糖皮质激素受体和热休克蛋白70在大鼠创伤失血性休克肝组织中的变化及其意义
引用本文:罗东林,周继红,刘宝华,熊仁平,叶秀峰,徐祥,陈金萍. 糖皮质激素受体和热休克蛋白70在大鼠创伤失血性休克肝组织中的变化及其意义[J]. 中国危重病急救医学, 2005, 17(11): 651-653
作者姓名:罗东林  周继红  刘宝华  熊仁平  叶秀峰  徐祥  陈金萍
作者单位:400042,重庆,第三军医大学大坪医院野战外科研究所四室,重庆医科大学病理教研室
基金项目:国家重点基础研究发展规划项目(G1999054200);重庆市自然科学基金资助项目(2004-BB5068)
摘    要:目的从组织细胞受体水平探讨糖皮质激素受体(GR)和热休克蛋白70(HSP70)在创伤失血性休克后肝脏中的变化及其作用。方法采用双侧股骨骨折伴失血性休克致严重创伤模型,动态观察伤后8h大鼠肝组织GR、HSP70、血清肝功能生化指标、肝脏病理等变化。采用蛋白质免疫印迹法(Western blot)测定肝组织GR、HSP70含量,并进行计算机图像分析。结果单纯股骨骨折伤后,肝组织GR含量于伤后1h即开始下降,6h降至最低,8h仍显著低于正常对照组;创伤合并休克后,GR下降更加明显。HSP70在单纯股骨骨折伤后迅速增加,6h达到峰值,8h仍持续在较高水平;创伤合并休克后,HSP70升高更加显著。单纯股骨骨折伤后,血清丙氨酸转氨酶(ALT)、总胆红素(TB)和白蛋白与正常对照组比较,差异均无显著性。但创伤合并休克后4h和2h血清ALT和TB分别开始明显增高(P均d〈0.01),白蛋白则均下降(P均〈0.01)。创伤合并休克后6h肝脏镜下肝窦内即出现较多炎性细胞浸润。结论GR不足在严重创伤失血性休克后肝脏继发性损害过程中起重要作用,HSP70可能参与了肝组织细胞抗损伤机制的启动。

关 键 词:创伤 休克 失血性 受体 糖皮质激素 热休克蛋白 肝损伤
收稿时间:2005-06-09
修稿时间:2005-10-28

Changes in glucocorticoid receptor and heat shock protein 70 in liver tissue after trauma with hemorrhagic shock in rats
LUO Dong-lin,ZHOU Ji-hong,LIU Bao-hua,XIONG Ren-ping,YE Xiu-feng,XU Xiang,CHEN Jin-ping. Changes in glucocorticoid receptor and heat shock protein 70 in liver tissue after trauma with hemorrhagic shock in rats[J]. Chinese critical care medicine, 2005, 17(11): 651-653
Authors:LUO Dong-lin  ZHOU Ji-hong  LIU Bao-hua  XIONG Ren-ping  YE Xiu-feng  XU Xiang  CHEN Jin-ping
Affiliation:Research Institute of Surgery, Daping Hospital, The Third Military Medical University, Chongqing 400042, China
Abstract:Objective To investigate changes and functions of glucocorticoid (GR) and heat shock protein 70 (HSP70) at the level of cellular receptor in liver in hemorrhagic shock after trauma. Methods Adult Wistar rats were used and a rat model of shock was reproduced by hemorrhaging accompanied by bilateral femur fracture. Changes in hepatic tissue GR, HSP70, pathology of liver, hepatic function markers in serum were dynamically observed. The expression of GR and HSP70 in hepatic tissue was assayed by Western blot and then analyzed with computer imaging system. Results Protein content of GR gradually decreased in hepatic tissue after trauma, reduced to the nadir at 6 hours after trauma, and it was decreased even more when trauma was added to bleeding. Protein content of HSP70 was gradually increased in hepatic tissue after severe trauma, peaking at 6 hours after trauma, and it maintained at a rather high level at 8 hours after trauma. It was even more increased in when hemorrhagic shock was followed by trauma. Alterations in hepatic function markers and pathology were not obvious after simple trauma. But after trauma was added to hemorrhagic shock, significant increase in alaine aminotransferase (ALT) and total bilirubin (TB) in serum was noted at 4 and 2 hours after trauma respectively (all P<0.01), and albumin content was obviously decreased (P<0.01). There were more inflammatory cell infiltration in hepatic sinusoids at 6 hours after trauma. Conclusion GR may play an important role in antiinjury mechanism of hepatic tissue cell after trauma with hemorrhagic shock. HSP70 may participate in initiating antiinjury mechanism of hepatic cells.
Keywords:trauma   hemorrhagic shock   glucocorticoid receptor    heat shock protein   liver injury
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