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Departments of *Anesthesiology and
Surgery, Tri-Service General Hospital; and Departments of
Biochemistry and
Physiology, National Defense Medical Center, Taipei, Taiwan, Republic of China
Address correspondence and reprint requests to Chi-Yuan Li, MD, MS, Department of Anesthesiology, #325 Section 2, Cheng-Kung Rd., Taipei, Taiwan, ROC. Address e-mail to cyli{at}ndmctsgh.edu.tw
It has been reported that, in patients with acute myocardial infarction or congestive heart failure, monocyte chemoattractant protein-1 (MCP-1) plays an important role in the development of inflammatory responses and that the level of MCP-1 is correlated with the severity of the disease. We conducted this study to investigate the effects of dobutamine and dopamine on lipopolysaccharide (LPS)-induced MCP-1 production in human monocytic THP-1 cells. Monocytes were incubated in vitro with LPS for 16 h at 37°C in the presence or absence of dobutamine or dopamine. Enzyme-linked immunosorbent assay was used to examine the effect of dobutamine on MCP-1 synthesis, with the MCP-1 messenger RNA expression examined by reverse transcriptase-polymerase chain reaction. Dobutamine inhibited LPS-induced production of MCP-1, as well as messenger RNA expression, in a dose-dependent manner, whereas dopamine had no significant effect. Furthermore, we demonstrated that dobutamine suppressed MCP-1-induced chemotaxis and peak [Ca2+]i in monocytic THP-1 cells. These findings suggest that dobutamine may modulate monocyte activation, such as chemotaxis and [Ca2+]i, as well as MCP-1 production, during therapy for congestive heart failure.
IMPLICATIONS: Monocyte chemoattractant protein-1 (MCP-1) plays important roles in the inflammatory processes associated with pathogenesis of cardiovascular diseases. In this study, dobutamine was found to inhibit lipopolysaccharide-induced MCP-1 production and messenger RNA expression, as well as MCP-1-induced chemotaxis and peak [Ca2+]i, in human monocytes.
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