KB-R7943 抑制高糖诱导的内皮细胞 ICAM-1 表达和单核细胞-内皮细胞黏附。
KB-R7943 inhibits high glucose-induced endothelial ICAM-1 expression and monocyte-endothelial adhesion.
机构信息
Department of Cardiac Care Unit, The First Affiliated Hospital of Harbin Medical University, and Department of Physiology, Harbin Medical University, Harbin 150001, China.
出版信息
Biochem Biophys Res Commun. 2010 Feb 19;392(4):516-9. doi: 10.1016/j.bbrc.2009.12.183. Epub 2010 Jan 22.
Hyperglycemia is the major cause of diabetic angiopathy. The aim of our study was to evaluate the impact of KB-R7943, an inhibitor of Na+/Ca2+ exchanger (NCX) on cell growth and function of human "diabetic" endothelial cells (EC). Intercellular adhesion molecule-1 (ICAM-1) expression and NCX activity were determined after EC were exposed to high glucose in the absence and presence of KB-R7943. Coincubation of EC with high glucose for 24 h resulted in a significant increase of monocyte-endothelial cell adhesion and the expression of ICAM-1. These effects were abolished by KB-R7943 and KB-R7943 significantly decreased the activation of NCX induced by high glucose. These findings suggested that KB-R7943 may play a role in inhibiting expression of adhesion molecules by inhibiting the reverse activation of NCX.
高血糖是糖尿病血管病变的主要原因。我们的研究目的是评估 Na+/Ca2+ 交换体（NCX）抑制剂 KB-R7943 对人“糖尿病”内皮细胞（EC）生长和功能的影响。在不存在和存在 KB-R7943 的情况下，将 EC 暴露于高葡萄糖中后，测定细胞间黏附分子-1（ICAM-1）表达和 NCX 活性。EC 与高葡萄糖共孵育 24 小时会导致单核细胞-内皮细胞黏附显著增加和 ICAM-1 表达增加。这些作用被 KB-R7943 消除，并且 KB-R7943 显著降低了高葡萄糖诱导的 NCX 的激活。这些发现表明，KB-R7943 可能通过抑制 NCX 的反向激活在抑制黏附分子的表达中发挥作用。
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