Homocysteine induces production of monocyte chemoattractant protein-1 and interleukin-8 in cultured human whole blood
Abstract
AIM:
To investigate whether increased plasma L-homocysteine (Hcy) level could promote monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) in cultured whole blood.
METHODS:
Human whole blood or different type of peripheral blood cells from health volunteers were incubated with Hcy and/or the inhibitors. MCP-1 and IL-8 level were measured by ELISA assay.
RESULTS:
Hcy 10-1000 micromol/L induced production of MCP-1 and IL-8 in cultured human whole blood (P<0.05). The major cellular source of these chemokines comed from monocytes. Meanwhile,Hcy also promoted the upregulation of MPO level even at the 10 micromol/L in the cultured whole blood. The intracellular ROS, particular the OH. radicals, play extremely important role in the Hcy-induced MCP-1 and IL-8 production.
CONCLUSION:
Increased Hcy level in plasma (hyperhomocysteinemia) induced MCP-1 and IL-8 secretion in cultured human whole blood, especially in monocytes via oxidative stress mechanism.
Keywords:
To investigate whether increased plasma L-homocysteine (Hcy) level could promote monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) in cultured whole blood.
METHODS:
Human whole blood or different type of peripheral blood cells from health volunteers were incubated with Hcy and/or the inhibitors. MCP-1 and IL-8 level were measured by ELISA assay.
RESULTS:
Hcy 10-1000 micromol/L induced production of MCP-1 and IL-8 in cultured human whole blood (P<0.05). The major cellular source of these chemokines comed from monocytes. Meanwhile,Hcy also promoted the upregulation of MPO level even at the 10 micromol/L in the cultured whole blood. The intracellular ROS, particular the OH. radicals, play extremely important role in the Hcy-induced MCP-1 and IL-8 production.
CONCLUSION:
Increased Hcy level in plasma (hyperhomocysteinemia) induced MCP-1 and IL-8 secretion in cultured human whole blood, especially in monocytes via oxidative stress mechanism.