Department of Exercise and Sport Physiology, Faculty of Sport Sciences, Hacettepe University, Ankara, Turkey.
Division of Cardiology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Cardiovasc Drugs Ther. 2023 Oct;37(5):1027-1029. doi: 10.1007/s10557-022-07344-w. Epub 2022 May 13.
Glucocorticoids, which are widely prescribed around the world, cause cardiac remodeling in long-term treatment by triggering insulin resistance and increasing blood pressure. However, its role in cardiac remodeling remains unclear. Galectin-3 (gal-3) is a member of a beta-galactoside-binding animal lectins, upregulated as a result of insulin resistance and in the pressure-overloaded myocardium and regulate cardiac remodeling. We hypothesized that gal-3 may be upregulated in the myocardium with prolonged use of glucocorticoids and associated with cardiac hypertrophy.
To examine the involvement of glucocorticoids in gal-3 levels in rat myocardium, sixteen female Wistar Albino rats were assigned to control (C; n = 8) and dexamethasone (Dex; n = 8) groups. Daily dexamethasone was injected subcutaneously for 28 days at a dose of 1 mg.kg. Control animals were injected with the same volume of saline. The body weight and heart weights were determined. Gal-3 levels in myocardium were determined by Western blot.
Our data shows that dexamethasone administration resulted in significant increase in heart weight (p < 0.05) and HW/BW ratios (p < 0.001) and 28 days of dexamethasone administration with the dose of 1 mg.kg caused a twofold increase in the gal-3 expression in the left ventricle (p < 0.001).
The finding of the current study is the first to show that dexamethasone causes an increase in gal-3 levels in myocardium. Our study provides an important step in the development of possible therapeutics by determining that dexamethasone causes an increase in gal-3 levels in the myocardium and raises awareness about the follow-up of patients receiving long-term glucocorticoid therapy.
糖皮质激素在全球范围内广泛应用，通过引发胰岛素抵抗和升高血压，在长期治疗中引起心脏重构。然而，其在心脏重构中的作用尚不清楚。半乳糖凝集素-3（gal-3）是一种β-半乳糖苷结合动物凝集素家族的成员，由于胰岛素抵抗和心脏压力超负荷而上调，并调节心脏重构。我们假设 gal-3 在长期使用糖皮质激素的心肌中可能上调，并与心肌肥厚有关。
为了研究糖皮质激素在大鼠心肌中 gal-3 水平的作用，将 16 只雌性 Wistar 白化大鼠分为对照组（C；n=8）和地塞米松组（Dex；n=8）。Dex 组每天经皮下注射地塞米松，剂量为 1mg.kg，共 28 天。对照组注射相同体积的生理盐水。测定体重和心脏重量。通过 Western blot 测定心肌中 gal-3 水平。
我们的数据表明，地塞米松给药导致心脏重量显著增加（p<0.05）和 HW/BW 比值显著增加（p<0.001），且 1mg.kg 的地塞米松剂量连续给药 28 天导致左心室 gal-3 表达增加两倍（p<0.001）。
本研究首次表明地塞米松导致心肌中 gal-3 水平升高。我们的研究通过确定地塞米松导致心肌中 gal-3 水平升高，为开发可能的治疗方法提供了重要步骤，并提高了对接受长期糖皮质激素治疗的患者进行随访的认识。
