Tanshinone IIA is one of the most predominant bioactive constituents of Danshen, a traditional Chinese medicinal plant with multiple cardiovascular protective actions. Although Tanshinone IIA has been well documented for its endothelial protective efficacy, studies unveiling the mechanism and/or molecular targets for its pharmacological activity are still inadequate. In recent studies, it has been envisaged that the expression of pentraxin 3 (PTX3) was associated with atherosclerotic cardiovascular diseases (ACVD). Therefore, the current study was designed to evaluate the possible role of Tanshinone IIA in influencing the expression of PTX3 in endothelial cells and thereby prevents endothelial dysfunction. Molecular analyses through real-time PCR, western blot, and ELISA revealed that Tanshinone IIA down-regulates PTX3 gene expression as well as protein secretion in human endothelial cells in the presence or absence of TNF-α. Besides, Tanshinone IIA inhibits the adhesion of THP1 cells (a monocytic cell line) to activated-endothelial cells stimulated with TNF-α. Furthermore, mechanistic studies uncovered the role of p38 MAPK/NF-κB pathway in Tanshinone II-A mediated pharmacological effects. Thus, the present study exemplifies the manifestation of Tanshinone IIA as a plausible alternative natural remedy for ACVD by targeting PTX3.

丹参酮IIA是丹参中最主要的生物活性成分之一，丹参是具有多种心血管保护作用的传统中草药。尽管丹参酮IIA具有良好的内皮保护功效，但有关其药理活性的机理和/或分子靶标的研究仍不充分。在最近的研究中，已经设想到戊糖毒素3（PTX3）的表达与动脉粥样硬化性心血管疾病（ACVD）有关。因此，当前的研究旨在评估丹参酮IIA在影响内皮细胞中PTX3表达从而预防内皮功能障碍中的可能作用。通过实时PCR，蛋白质印迹，ELISA和ELISA显示，在存在或不存在TNF-α的情况下，丹参酮IIA下调人内皮细胞中PTX3基因的表达以及蛋白质分泌。此外，丹参酮IIA抑制THP1细胞（单核细胞系）与TNF-α刺激的活化内皮细胞的粘附。此外，机理研究揭示了p38 MAPK /NF-κB途径在丹参酮II-A介导的药理作用中的作用。因此，本研究通过靶向PTX3举例说明了丹参酮IIA作为ACVD的可行替代天然药物的表现。机理研究揭示了p38 MAPK /NF-κB通路在丹参酮II-A介导的药理作用中的作用。因此，本研究通过靶向PTX3举例说明了丹参酮IIA作为ACVD的可行替代天然药物的表现。机理研究揭示了p38 MAPK /NF-κB通路在丹参酮II-A介导的药理作用中的作用。因此，本研究通过靶向PTX3举例说明了丹参酮IIA作为ACVD的可行替代天然药物的表现。