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    Long-term Dexamethasone Treatment Increases Cardiac Galectin-3 Levels
    (Springer, 2023) Akin, Senay; Gucuk-Ipek, Esra; Hayta, Umit; Gungor, Irem; Kubat, Gokhan Burcin; Akin, Yesim; Guray, Umit
    Purpose 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. Methods 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(-1). 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. Results 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(-1) caused a twofold increase in the gal-3 expression in the left ventricle (p < 0.001). Conclusion 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.