Huang Jiangyan, Yang Qin, He Longmiao, Huang Jun
Department of Cardiology, First Affiliated Hospital, Nanchang University, Nanchang, China.
J Clin Lab Anal. 2018 Feb;32(2). doi: 10.1002/jcla.22232. Epub 2017 Apr 13.
To study the role of toll-like receptor 4 (TLR4) and MicroRNA-155 (miR-155) in the peripheral blood mononuclear cell (PBMC)-mediated inflammation in coronary slow flow (CSF) and coronary arteriosclerosis.
Patients were divided into acute coronary syndrome (ACS), stable angina pectoris (SAP), CSF, and healthy control (HC) groups. The isolated PBMCs were treated with lipopolysaccharide (LPS)/and antagomiR-155. TLR4, miR-155, and the concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1, and IL-10 were measured.
Before LPS intervention, the TLR4, TNF-α, IL-1, and IL-6 levels were higher and the level of miR-155, IL-10 was lower in the ACS group compared with the SAP, CSF, and HC groups. After exposure to LPS, the levels of TLR4, miR-155, TNF-α, IL-1, and IL-6 were increased and the level of IL-10 was decreased in the SAP and CSF groups compared with the HC group. But when over-expressing antagomiR-155 into PBMCs from SAP and CSF groups, the miR-155 expression, and TNF-α, IL-6, and IL-1 secretion increase induced by LPS were restrained.
TLR4, miR-155, and inflammatory cytokines may be closely related to ACS. LPS can induce TLR4, miR-155 expression and inflammatory response in SAP and CSF patients. AntagomiR-155 can inhibit this inflammatory response.
研究Toll样受体4（TLR4）和微小RNA-155（miR-155）在冠状动脉慢血流（CSF）和冠状动脉粥样硬化外周血单个核细胞（PBMC）介导的炎症中的作用。
将患者分为急性冠状动脉综合征（ACS）、稳定型心绞痛（SAP）、CSF和健康对照（HC）组。分离的PBMC用脂多糖（LPS）/和抗miR-155处理。检测TLR4、miR-155以及肿瘤坏死因子（TNF）-α、白细胞介素（IL）-6、IL-1和IL-10的浓度。
在LPS干预前，与SAP、CSF和HC组相比，ACS组的TLR4、TNF-α、IL-1和IL-6水平较高，而miR-155、IL-10水平较低。暴露于LPS后，与HC组相比，SAP和CSF组的TLR4、miR-155、TNF-α、IL-1和IL-6水平升高，而IL-10水平降低。但是，当将抗miR-155过表达于SAP和CSF组的PBMC中时，LPS诱导的miR-155表达以及TNF-α、IL-6和IL-1分泌增加受到抑制。
TLR4、miR-155和炎性细胞因子可能与ACS密切相关。LPS可诱导SAP和CSF患者的TLR4、miR-155表达及炎症反应。抗miR-155可抑制这种炎症反应。
