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Hemolysate-induced expression of intercellular adhesion molecule-1 and monocyte chemoattractant protein-1 expression in cultured brain microvascular endothelial cells via through ROS-dependent NF-kappaB pathways. | LitMetric

AI Article Synopsis

  • The study investigates how hemolysate affects brain microvascular endothelial cells (BMECs), focusing on inflammatory markers like ICAM-1 and MCP-1.
  • Hemolysate was found to increase the expression of these markers, stimulate NF-kappaB activation, and enhance the generation of reactive oxygen species (ROS) in BMECs.
  • The findings suggest that hemolysate triggers inflammatory responses in BMECs through a mechanism involving ROS and NF-kappaB activation.

Article Abstract

In order to determine the possible effects of hemolysate on brain microvascular endothelial cells (BMECs), we examined the effects of hemolysate on the expression of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1), generation of reactive oxygen species (ROS), and NF-kappaB activation in rat BMECs. Hemolysate induced the expression of ICAM-1 and MCP-1 in endothelial cells. In addition, hemolysate stimulated nuclear translocation of the p65 subunit of NF-kappaB, and NF-kappaB DNA-binding activity in BMECs. Furthermore, hemolysate increased ROS generation, and hemolysate-induced ICAM-1and MCP-1 expression and NF-kappaB activation were abrogated in the presence of the direct scavenger of ROS. Taken together, our results indicate that hemolysate can induce inflammatory responses that increase expression of ICAM-1 and MCP-1, through ROS-dependent NF-kappaB activation in BMECs.

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Source
http://dx.doi.org/10.1007/s10571-008-9300-3DOI Listing

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