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参麦注射液预先给药对心肌缺血-再灌注损伤大鼠心肌HMGB-1表达的作用 被引量:15

Effects of pre-injection Shenmai on cardiac HMGB-1 in myocardial ischemia-reperfusion injury rats
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摘要 目的研究参麦注射液对心肌缺血-再灌注损伤大鼠心肌组织高迁移率族蛋白B1(HMGB-1)表达的作用。方法取30只SD大鼠随机均分为假手术组(Sham组)、心肌缺血-再灌注未干预组(IR组)、参麦注射液组(SM组),SM组每天腹腔内注射参麦注射液10ml/kg,连续3d,Sham组及IR组则按同样方法注射等容量生理盐水。Sham组分离左冠状动脉前降支,穿线后不结扎;IR及SM组开胸结扎左冠状动脉前降支,造成心肌缺血,30min后放松再灌注60min,建立心肌缺血-再灌注模型。ELISA法检测心肌组织HMGB-1的表达。显微镜下观察缺血心肌超微结构变化。结果与Sham组比较,IR组和SM组大鼠心肌组织HMGB-1含量明显增高(P<0.01)。与IR组相比,SM组大鼠心肌组织HMGB-1含量显著降低(P<0.01)。IR组心肌超微结构明显受损,SM组受损较轻。结论参麦注射液可降低缺血-再灌注损伤后大鼠心肌组织HMGB-1的表达水平,抑制炎症反应,减轻心肌缺血-再灌注损伤,保护心肌。这种作用可能与参麦注射液对炎症介质HMGB-1的基因表达和胞外释放具有明显抑制作用有关。 Objective To investigate the effect of Shenmai injection on cardiac high mobility group boxl (HMGB-1) in myocardial ischemia-reperfusion injury rats. Methods Thirty heathy male SD rats were randomly divided into three groups(n: 10, each): Sham-operation(group Sham), ischemia and reperfusion (group IR), and Shenmai injection treatment (group SM), then 10 ml/kg Shenmai injection were given in group SM and the 0. 9% NaC1 10 ml/kg were given in groups Sham and IR group for three days. After thoracotomy and ligation, the rats were injured by ischemia and relaxed 30 minutes later, then reperfusioned for 60 minutes, the myocardial ischemia-reperfusion models in rats were established during the experiment. The expressions of HMGB-1 was evaluated by ELISA. The myocardial samples were obtained for ultrastructure observation. Results Compared with group Sham, the expression level of HMGPrl in groups IR and SM were increased significantly (P〈0.01). Compared with group IR, the expression level of HMGB-1 from myocardial in group SM were decreased significantly (P〈0.01). Microscopic examination showed that myocardial ultrastructure in group SM was more slightly damaged than that in group IR. Conclusion These data suggest that: The expressions of HMGB-1 were increased significantly in ischemia-reperfused myocardial (MIR) rats. Shenmai injection can greatly depressed expression of HMGB-1. Shenmai injection may reduce systemic inflammatory response and protect myocardium ischemia/reperfusion injury. Inhibitory of HMGB-1 release may be the possible therapeutic mechanisms.
出处 《临床麻醉学杂志》 CAS CSCD 北大核心 2012年第11期1102-1104,共3页 Journal of Clinical Anesthesiology
基金 江苏大学临床医学科技发展基金项目(JLY2010236) 江苏省镇江市社会发展科技支撑项目(SH2010014)
关键词 缺血-再灌注损伤 高迁移率族蛋白-B1 参麦注射液 Ischemia-reperfusion injury High mobility group box 1 Shenmai injection
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参考文献9

  • 1Singla DK, Hacker TA, Ma L, et al. Transplantation of em- bryonic stem cells into the infarcted mouse heart formation of multiple cell types. J Mol Cell Cardiol, 2006, 40 (1): 195-200.
  • 2Lotze MT, Tracey KJ. High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal. Nat Rev Immunol, 2005,5 (4) : 331-342.
  • 3温晓竞,朱秀燕,张敏,焦宏,马建伟,陈彦静.参麦注射液对大鼠心肌缺血再灌注中一氧化氮、一氧化氮合酶和内皮素的影响[J].陕西中医,2009,30(12):1680-1681. 被引量:14
  • 4Rowe DC,McGettrick AF,Latz E,et al. The myristoylation of TRIF-related adaptor molecule is essential for Toll-like recep- tor 4 signal transduction. Proe Natl Aead Sci U S A, 2006, 103(16) .. 6299-6304.
  • 5谷腾飞,赵明,蒋鹏,王珊珊.参麦注射液对缺血-再灌注损伤大鼠心肌H-FABP和血清FFA的影响[J].临床麻醉学杂志,2011,27(6):590-592. 被引量:7
  • 6; Karlsson S, Pettila V, Tenhunen J, et al. HMGB1 as a pre- dictor of organ dysfunction and outcome in patients with severe sepsis. Intensive Care Med, 2008, 34(6) .. 1046-1053.
  • 7Herold K, Moser B, Chen Y, et al. Receptor for advanced glycation end products(RAGE) in a dash to the rescue:inflam- matory signals gone awry in the primal response to stress. J Leukoc Biol, 2007, 82(2) : 204-212.
  • 8Oozawa S,Moris S, Kanke T, et al. Effects of HMGB1 on is- chemia/reperfusion injury in the rat heart. Circ J, 2008, 72 (7): 1178-1184.
  • 9Hu X, Jiang H, Cui B, et al. Preconditioning with high mob- ility group box 1 protein protects against myocardial ischemia- reperfusion injury. Int J Cardiol, 2010,145(1) : 111-112.

二级参考文献14

  • 1郭群,陈水英,张作明,姚秀娟.心肌缺血-再灌注损伤与氧自由基关系的研究[J].陕西医学杂志,2006,35(8):932-933. 被引量:10
  • 2张冰,李莉,田临红.参麦注射液的临床应用进展[J].现代中西医结合杂志,2007,16(10):1444-1445. 被引量:28
  • 3Seddon M, Shah AM, Casadei B. Cardiomyocytes as effectors of nitric oxide signaling. Cardiovase Res, 2007, 75 (2):315-326.
  • 4Hannan RL, John MC, Kouretas PC, et al. Deletion of endothelial nitric oxide synthase exacerbates myocardial stunning in an isolated mouse heart model [J]. J Surg Res, 2000, 93(1):127-132.
  • 5Maczewski M, Beresewicz A. The role of endothelin, protein kinase C and free radicals in the mechanism of the post-ischemic endothelial dysfunction in guinea-pig hearts[J]. J Mol Cell Cardiol, 2000, 32(2):297-310.
  • 6Buja LM. Myocardial ischemia and reperfusion injury. Cardio- vasc Pathol, 2005,14 : 170-175.
  • 7Luiken J, Koonen D, Coumans W, et al. Long-chain fatty acid up take by skeletal muscle is impaired in homozygous, but not heterozygous heart type-FABP null mice. Lipids, 2003, 38: 491-496.
  • 8Meng X, Ming M, Wang E. Heart fatty acid binding protein as a marker for postmortem detection of early myocardial damage. Forensic Science Internationah2006,160:11-16.
  • 9柯柳,余叶蓉,张玄娥,张祥迅,陆志明.高游离脂肪酸血症对心肌结构与功能的影响及其机制[J].四川大学学报(医学版),2009,40(1):24-28. 被引量:30
  • 10赵明,蒋鹏,刁玉晶,汪小海.参麦注射液对控制性低温家兔血液流变学的影响[J].临床麻醉学杂志,2009,25(10):891-893. 被引量:1

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