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Clinical significance of serum MCP-1 and VE-cadherin levels in patients with acute cerebral infarction.
European Review for Medical and Pharmacological Sciences 2017 Februrary
OBJECTIVE: Vascular injuries have been proposed to play a role in cerebral infarction (CI)-induced brain damage. In this study, the expressions of monocyte chemoattractant protein-1 (MCP-1) and vascular endothelial-cadherin (VE-Cadherin) in patients with acute stroke was examined, and the clinical significance was analyzed.
PATIENTS AND METHODS: 102 patients with acute CI between February 2012 and 2015 were recruited in this study. Among these patients, 43 patients presented with progressive cerebral infarction (PCI) while 59 patients presented with non-progressive cerebral infarction (NPCI). The carotid intima-media thickness (IMT) of all patients was measured by ultrasound as a marker of end-organ damage. Our results showed that 26 patients had normal IMT, 19 patients had a thickening carotid wall and 57 patients presented with a carotid plaque. In our study, 52 healthy volunteers screened by medical checkups in our hospital during the same period were taken as control group. The MCP-1 and VE-cadherin expressions in each group were detected and analyzed.
RESULTS: Compared to the control group, the patients in the experimental group had significantly elevated serum MCP-1 and VE-cadherin levels (p < 0.05). Compared to the NPCI patients, the serum MCP-1 and VE-cadherin levels of the patients with PCI were significantly increased, and the rate of carotid plaque was increased as well, especially in the mixed echo and low echo plaques. Then compared with the patients with normal IMT and thickening carotid wall, the patients with carotid plaques had notably increased MCP-1 and VE-cadherin levels.
CONCLUSIONS: For patients with PCI, the serum MCP-1 and VE-cadherin levels were significantly increased. Moreover, serum MCP-1 and VE-cadherin levels were correlated with atherosclerosis and the stability of atherosclerotic plaques in patients with cerebral infarction.
PATIENTS AND METHODS: 102 patients with acute CI between February 2012 and 2015 were recruited in this study. Among these patients, 43 patients presented with progressive cerebral infarction (PCI) while 59 patients presented with non-progressive cerebral infarction (NPCI). The carotid intima-media thickness (IMT) of all patients was measured by ultrasound as a marker of end-organ damage. Our results showed that 26 patients had normal IMT, 19 patients had a thickening carotid wall and 57 patients presented with a carotid plaque. In our study, 52 healthy volunteers screened by medical checkups in our hospital during the same period were taken as control group. The MCP-1 and VE-cadherin expressions in each group were detected and analyzed.
RESULTS: Compared to the control group, the patients in the experimental group had significantly elevated serum MCP-1 and VE-cadherin levels (p < 0.05). Compared to the NPCI patients, the serum MCP-1 and VE-cadherin levels of the patients with PCI were significantly increased, and the rate of carotid plaque was increased as well, especially in the mixed echo and low echo plaques. Then compared with the patients with normal IMT and thickening carotid wall, the patients with carotid plaques had notably increased MCP-1 and VE-cadherin levels.
CONCLUSIONS: For patients with PCI, the serum MCP-1 and VE-cadherin levels were significantly increased. Moreover, serum MCP-1 and VE-cadherin levels were correlated with atherosclerosis and the stability of atherosclerotic plaques in patients with cerebral infarction.
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