Department of Cardiac Surgery, Innsbruck Medical University, Innsbruck, Austria.
Inflammation. 2014 Feb;37(1):65-70. doi: 10.1007/s10753-013-9712-1.
Shock wave therapy (SWT) reportedly improves ventricular function in ischemic heart failure. Angiogenesis and inflammation modulatory effects were described. However, the mechanism remains largely unknown. We hypothesized that SWT modulates inflammation via toll-like receptor 3 (TLR3) through the release of cytosolic RNA. SWT was applied to human umbilical vein endothelial cells (HUVECs) with 250 impulses, 0.08 mJ/mm(2) and 3 Hz. Gene expression of TLR3, inflammatory genes and signalling molecules was analysed at different time points by real-time polymerase chain reaction. SWT showed activation of HUVECs: enhanced expression of TLR3 and of the transporter protein for nucleic acids cyclophilin B, of pro-inflammatory cytokines cyclophilin A and interleukin-6 and of anti-inflammatory interleukin-10. No changes were found in the expression of vascular endothelial cell adhesion molecule. SWT modulates inflammation via the TLR3 pathway. The interaction between interleukin (IL)-6 and IL-10 in TLR3 stimulation can be schematically seen as a three-phase regulation over time.
冲击波疗法（SWT）据称可改善缺血性心力衰竭的心室功能。描述了血管生成和炎症调节作用。然而，其机制在很大程度上尚不清楚。我们假设，SWT 通过释放细胞质 RNA 通过 Toll 样受体 3（TLR3）来调节炎症。用 250 个脉冲、0.08 mJ/mm(2) 和 3 Hz 的强度对人脐静脉内皮细胞（HUVEC）应用 SWT。通过实时聚合酶链反应在不同时间点分析 TLR3、炎症基因和信号分子的基因表达。SWT 显示出 HUVEC 的激活：TLR3 及其核酸转运蛋白亲环蛋白 B、前炎性细胞因子亲环蛋白 A 和白细胞介素-6 以及抗炎性白细胞介素-10 的表达增强。血管内皮细胞黏附分子的表达没有变化。SWT 通过 TLR3 途径调节炎症。TLR3 刺激中白细胞介素（IL）-6 和 IL-10 之间的相互作用可以示意性地看作是随时间的三相调节。
