Interaction between Kupffer cells and platelets in the early period of hepatic ischemia-reperfusion injury--an in vivo study.
Interaction between Kupffer cells and platelets in the early period of hepatic ischemia-reperfusion injury--an in vivo study.
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DOI：
10.1016/j.jss.2011.12.010
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发表时间：
2012-11
期刊：
影响因子：
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通讯作者：
Takafumi Tamura;T. Kondo;Sugiru Pak;Y. Nakano;S. Murata;K. Fukunaga;N. Ohkohchi
中科院分区：
文献类型：
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作者：
Takafumi Tamura;T. Kondo;Sugiru Pak;Y. Nakano;S. Murata;K. Fukunaga;N. Ohkohchi
肝缺血再灌注（I/R）导致枯否细胞（KCs）活化。活化的KCs引起血小板和白细胞粘附到窦内皮。以前，我们报道血小板-内皮细胞相互作用发生早于白细胞反应。本研究的目的是评估血小板和KCs之间的相互作用，在肝微循环I/R后。材料和方法Sprague-Dawley大鼠分为三组：无缺血组（对照组; n = 6），缺血20分钟组（I/R组; n = 6）和缺血20分钟+抗大鼠血小板血清组（APS组; n = 6）。采用脂质体包埋法标记KCs。在再灌注后120分钟内，通过活体显微镜观察粘附血小板的数量。为探讨血小板在I/R损伤中的作用，采用兔APS静脉注射法去除大鼠血小板，结果表明：I/R组大鼠I/R后粘附血小板数明显增加; 50%以上的粘附血小板粘附于KCs。电镜观察显示，肝缺血后，血小板粘附于KCs上。组织学结果表明，肝损伤和1区肝细胞凋亡。在I/R组，而不是在对照组和APS组，血清ALT升高后立即reperfusion. CONCLUSION我们成功地在可视化的动态KCs和血小板在肝窦。肝缺血早期诱导血小板与KCs粘附，在肝脏再灌注损伤中起重要作用。
BACKGROUNDHepatic ischemia–reperfusion (I/R) leads to activation of Kupffer cells (KCs). The activated KCs cause platelet and leukocyte adhesion to the sinusoidal endothelium. Previously, we reported that platelet–endothelium interactions occur earlier than leukocyte responses. The aim of this study was to evaluate the interaction between platelets and KCs in the hepatic microcirculation after I/R.MATERIALS AND METHODSSprague-Dawley rats were divided into three groups: the no-ischemia group (control group; n = 6); the 20-min ischemia group (I/R group; n = 6); and the 20-min ischemia + anti-rat platelet serum group (APS group; n = 6). KCs were labeled using the liposome entrapment method. The number of adherent platelets was observed for up to 120 min after reperfusion by intravital microscopy. To investigate the effects of platelets on I/R injury, rats were injected intravenously with rabbit APS for platelet depletion.RESULTSIn the I/R group, the number of adherent platelets increased significantly after I/R. More than 50% of the adherent platelets adhered to KCs. Electron microscopy indicated that the platelets attached to the KCs after hepatic ischemia. The histologic findings indicated liver damage and apoptosis of hepatocytes in zone 1. In the I/R group, but not in the control and APS groups, serum ALT increased immediately after reperfusion.CONCLUSIONSWe succeeded in visualizing the dynamics of both KCs and platelets in the hepatic sinusoids. Liver ischemia induced the adhesion of platelets to KCs in the early period, which could play a key role in reperfusion injury of the liver.