New myocardial motection with cytokine network.

细胞因子网络的新心肌运动。

• 批准号: 05454386
• 负责人: NAKANO Susumu
• 金额: $ 4.42万
• 依托单位: Osaka University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (B)
• 财政年份: 1993
• 资助国家: 日本
• 起止时间: 1993 至 1994
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-05454386/
• 关键词: Reperfusion; Neutrophil; Cytokine; Myocyte; Endothelial cell; Adhesion; Migration; Free radical; neutrophil; Cytolsine; Adhesir; Free Radical; Neutrophil

To elucidate the mechanism of neutrophil(Np) induced reperfusion injury in myocardium, Np myocytes(Mc) and endothelial cells(Ec) were isolated from adult rat heart and blood. To elucidate the hypothesis that Np plays a role in reperfusion injury, a coincubation system with a monolayr of endothelial cells on the collagen membrane and myocytes under a collagen membrane was established. In this system, significant increase of Np migration through Ec, Mc damage and count of chemiluminescence were increased by 2 hours of hypoxia.However, these changes were decreased by administration of monoclonal antibody anti ICAM-1 and IL-6. Hypoxic Mc and Ec showed significant expression of ICAM-1. In the supernatant of hypoxic myocyte, significant increase of IL-6 was detected as compared to normoxic myocytes. These results suggested that ICAM-1 on Ec and Mc is implicated in Np migration through Ec and Np induced damage resulting in the extension of reperfusion injury in myocardium. Moreover, IL-6 may be derived from hypoxic myocytes and promote neutrophil induced reperfusion injury.

为了阐明嗜中性粒细胞（NP）诱导的心肌中的再灌注损伤，从成年大鼠心脏和血液中分离出NP心肌细胞（MC）和内皮细胞（EC）。为了阐明NP在再灌注损伤中发挥作用的假设，建立了与胶原膜上的内皮细胞单层的共同结合系统，并在胶原膜下建立了肌细胞。在该系统中，NP通过EC的迁移显着增加，MC损伤和化学发光的计数增加了2小时的缺氧。但是，通过施用单克隆抗体抗ICAM-ICAM-1和IL-6，这些变化减少了。缺氧MC和EC显示出ICAM-1的显着表达。在低氧肌细胞的上清液中，与常氧性肌细胞相比，检测到IL-6的显着增加。这些结果表明，EC和MC上的ICAM-1与NP通过EC和NP诱导的损伤有关，从而导致心肌中再灌注损伤扩大。此外，IL-6可以源自低氧肌细胞并促进中性粒细胞诱导的再灌注损伤。