AIMS The expression of cell adhesion molecules on vascular smooth muscle cells is central to leukocyte recruitment and progression of atherosclerotic disease. Ohioensin F, a chemical compound of the Antarctic moss Polyerichastrum alpinum, exhibited inhibitory activity against protein tyrosine phosphatase 1B and antioxidant activity. However, published scientific information regarding other biological activities and pharmacological function of ohioensin F is scarce. In the present study, we aimed to examine the in vitro effects of ohioensin F on the ability to suppress TNF-α-induced adhesion molecule expression in vascular smooth muscle cells (VSMCs). MAIN METHODS The inhibitory effect of ohioensin F on TNF-α-induced upregulation in expression of adhesion molecules was investigated by enzyme-linked immunosorbent assay, cell adhesion assay, RT-PCR, western blot analysis, immunofluorescence, and transfection and reporter assay, respectively. KEY FINDINGS Pretreatment of VSMCs with ohioensin F at nontoxic concentrations of 0.1-10 μg/ml dose-dependently inhibited TNF-α-induced expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). In addition, ohioensin F suppressed adhesion of THP-1 monocytes to TNF-α-stimulated VSMCs. Ohioensin F reduced TNF-α-induced production of intracellular reactive oxygen species (ROS) and phosphorylation of p38, ERK, JNK and Akt. Finally, ohioensin F inhibited TNF-α-induced CAM mRNA expression and NK-κB translocation. SIGNIFICANCE These results suggest a new mechanism of ohioensin F's anti-inflammatory action, owing to the negative regulation of TNF-α-induced adhesion molecule expression, monocyte adhesion and ROS production in vascular smooth muscle cells. Our finding also supports ohioensin F as a potential pharmacological, anti-inflammatory molecule that has a protective effect on the atherosclerotic lesion.

中文翻译：

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俄亥俄菌素F通过失活血管平滑肌细胞中的MAPK，Akt和NF-κB途径来抑制TNF-α诱导的粘附分子表达。

目的血管平滑肌细胞上细胞粘附分子的表达对于白细胞募集和动脉粥样硬化疾病的进展至关重要。Ohioensin F，一种南极苔藓植物多鞭毛虫的化合物，对蛋白酪氨酸磷酸酶1B具有抑制活性，并具有抗氧化活性。但是，关于卵菌素F的其他生物学活性和药理功能的公开科学信息很少。在本研究中，我们旨在检查卵磷脂在抑制血管平滑肌细胞（VSMC）中TNF-α诱导的黏附分子表达的能力方面的体外作用。主要方法通过酶联免疫吸附测定，细胞黏附测定，RT-PCR，研究卵磷脂F对TNF-α诱导的黏附分子表达上调的抑制作用。蛋白质印迹分析，免疫荧光，转染和报告基因检测。主要发现用无毒浓度0.1-10μg/ ml的卵磷脂F预处理VSMC剂量依赖性地抑制TNF-α诱导的血管细胞粘附分子1（VCAM-1）和细胞间粘附分子1（ICAM-1）的表达）。此外，卵磷脂O抑制THP-1单核细胞与TNF-α刺激的VSMC的粘附。俄亥俄霉素F降低了TNF-α诱导的细胞内活性氧（ROS）的产生以及p38，ERK，JNK和Akt的磷酸化。最后，卵磷脂F抑制TNF-α诱导的CAM mRNA表达和NK-κB易位。意义这些结果表明，由于TNF-α诱导的黏附分子表达的负调控，卵磷脂F的抗炎作用的新机制，血管平滑肌细胞中的单核细胞粘附和ROS产生。我们的发现还支持卵磷脂O作为潜在的药理抗炎分子，对动脉粥样硬化病变具有保护作用。