Department of Physiology and Morphology, Institute of Medicinal Chemistry, Hoshi University, Shinagawa-ku, Tokyo, 142-8501, Japan.
Second Department of Pharmacology, School of Pharmaceutical Sciences, Kyushu University of Medical Science, 1714-1 Yoshino-cho, Nobeoka, 882-8508, Miyazaki, Japan.
Sci Rep. 2024 Nov 1;14(1):26266. doi: 10.1038/s41598-024-78321-6.
Endothelial dysfunction exacerbates hypertension and other vascular complications in diabetes mellitus (DM). Circulating microparticles (MPs) and extracellular vesicles released in patients with DM have emerged as novel regulators of endothelial dysfunction. The obstruction of mineralocorticoid receptors (MRs) is a potential therapeutic approach to reduce cardiovascular complications. Their impact on the obstruction of MRs on circulating MPs and endothelial dysfunction in DM remains unclear. DM was induced in mice through a single intravenous dose of streptozotocin (STZ; 200 mg/kg). Esaxerenone (ESAX; 3 mg/kg/day), a MR blocker was administered via diet for 8 weeks. In this study, the aortas of the DM group showed the endothelial dysfunction and the administration of ESAX ameliorated the endothelial-dependent responses. Moreover, ESAX influences the impaired endothelial-dependent responses of DM-derived MPs. Interestingly, MP levels increased in DM whereas decreased after ESAX administration. In the aorta, the DM-derived MPs increased the expression of intercellular adhesion molecule-1 (ICAM-1). ESAX inhibited the adhesion of DM-derived MPs. Moreover, the ICAM-1 inhibitor A205804 shows similar effects as ESAX. These results indicate that the release and adhesion properties of MPs can be partially obstructed by ESAX via the ICAM-1 signaling pathway, which clarifies the other functions beyond the anti-hypertensive effects of ESAX.
内皮功能障碍会加重糖尿病(DM)患者的高血压和其他血管并发症。在 DM 患者中释放的循环微粒(MPs)和细胞外囊泡已成为内皮功能障碍的新型调节因子。阻断盐皮质激素受体(MRs)是减少心血管并发症的一种潜在治疗方法。它们对阻断 MRs 对 DM 中循环 MPs 和内皮功能障碍的影响尚不清楚。通过单次静脉注射链脲佐菌素(STZ;200mg/kg)诱导小鼠发生 DM。通过饮食给予 MR 阻滞剂依沙贝伦(ESAX;3mg/kg/天)8 周。在这项研究中,DM 组的主动脉表现出内皮功能障碍,而 ESAX 的给药改善了内皮依赖性反应。此外,ESAX 影响 DM 来源 MPs 的受损内皮依赖性反应。有趣的是,MP 水平在 DM 中增加,而在用 ESAX 给药后降低。在主动脉中,DM 来源的 MPs 增加了细胞间黏附分子-1(ICAM-1)的表达。ESAX 抑制 DM 来源 MPs 的黏附。此外,ICAM-1 抑制剂 A205804 显示出与 ESAX 相似的效果。这些结果表明,ESAX 通过 ICAM-1 信号通路部分阻断 MPs 的释放和黏附特性,这阐明了 ESAX 除了降压作用之外的其他功能。