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The role of TLR4 on mononuclear cell mediated inflammatory reaction in patients with coronary arteriosclerosis disease |
Huang Jun,He Long- miao,Yang Qin,Chen Yun- xiao |
Cardiology Department,the First Affiliated Hospital of Nanchang University,Nanchang 330006,China |
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Abstract Objective The study aims to explore toll-like receptor 4(TLR4)on peripheral blood mononuclear cell mediated inflammatory reaction in patients with coronary arteriosclerosis disease and coronary slow flow. Methods Patients were selected and divided into acute coronary syndrome (ACS)group,stable angina pectoris(SAP)group,coronary slow flow(CSF)group and healthy control (HC)group. Twenty ml blood was collected to separate the mononuclear cells using Lymphocytes Sepa⁃ ration Medium. The mononuclear cells were intervened with lipopolysaccharide(LPS)and/or atorvas⁃ tatin. The expression of TLR4 on peripheral blood mononuclear cell was analyzed by flow cytometry and the concentration of tumor necrosis factor(TNF)-α,interleukin(IL)-6,IL-1 and IL-10 in plasma or culture medium were measured by enzyme linked immunosorbent assay(ELISA). Results Before in⁃ tervention,the levels of TLR4,TNF-α,IL-1 and IL-6 were significantly higher,but the level of IL-10 was significantly lower from in the ACS group compared with the SAP,CSF and HC groups. The expres⁃ sions of TLR4,TNF-α,IL-1 and IL-6 were significantly increased,but the levels of IL-10 was signifi⁃ cantly decreased in the SAP and CSF groups after LPS stimulation,compared with HC group. Thesechanges can be reversed by atorvastatin intervention. Conclusion The results suggest that over-expres⁃ sion of TLR4 and inflammatory cytokines could be closely related to ACS. LPS can induce TLR4 of pe⁃ ripheral blood mononuclear cell mediated inflammatory response in patients with stable angina and coro⁃ nary slow flow. Atorvastatin can inhibit the over-expression of TLR4 and this inflammatory response.
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Received: 09 January 2016
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