中文摘要：

目的探讨线粒体钙稳态失衡在高尿酸（UA）导致的血管内皮细胞炎症中的病理生理机制。方法采用Fluo-3 AM及Rhod-2 AM分别对UA刺激后的人脐静脉内皮细胞（HUVEC-C）进行胞质钙离子浓度（[Ca2＋]i）和线粒体钙离子浓度（[Ca2＋]mito）的特异性染色;RT-PCR法检测其C反应蛋白（CRP）和细胞间黏附分子1（ICAM-1）的mRNA表达变化;Western blot检测ICAM-1的蛋白变化;ELISA法检测其培养液上清白细胞介素6（IL-6）的释放变化情况。结果HUVEC-C经600μmol/L的UA刺激后,其[Ca2＋]i未见明显变化,而[Ca2＋]mito呈波浪式升高（P〈0.05）,并在24 h内保持较高的状态;CRP、ICAM-1、IL-6均在UA刺激后升高（P〈0.05）。结论UA可导致内皮细胞炎症反应,[Ca2＋]mito的升高与之相关,提示线粒体钙稳态失衡在UA导致的内皮炎症反应中起一定的介导作用。

英文摘要：

Objective To evaluate the characteristics and mechanism of mitochondrial calcium homeostasis imbalance in vascular endothelial cells inflammation induced by uric acid.Methods Fluo-3 AM and Rhod-2 AM were employed to measure the introcellular calcium concentration（i） and mitochondrial calcium concentration（mito） of human umbilical vein endothelial cells（HUVEC-C） after stimulation of UA,respectively.RT-PCR was used to detected C-reactive protein（CRP） and the intercellular adhesion molecule-1（ICAM-1） levels of mRNA expression.Western blot was used to detect the ICAM-1 protein levels and ELISA was used to detect the culture medium on the innocence interleukin-6（IL-6） changes.Results After stimulation of 600 μmol/L of UA,the i of HUVEC-C was not changed significantly;however,the mito increased rapidly in a conk manner（P0.05） and it maintained as a relative high state in 24 hours.CRP,ICAM-1 and IL-6 were significantly increased after stimulation of UA（P0.05）.Conclusion Uric acid can lead to endothelial cell inflammatory response,which may be related to the increasing of mito in HUVEC-C.Mitochondrial calcium homeostasis imbalance was involved in endothelial inflammatory response induced by uric acid.