Empagliflozin Improves Endothelial Function in an Ovariectomized Rat Model of Estrogen Deficiency
Abstract
Cardiovascular disease risk increases after menopause, largely driven by estrogen deficiency-induced endothelial dysfunction. While sodium-glucose cotransporter 2 (SGLT2) inhibitors confer cardiovascular protection, their vascular effects under estrogen-deficient conditions remain unclear. This study investigated the effects of the SGLT2 inhibitor empagliflozin on vascular function in an ovariectomized (OVX) rat model of estrogen deficiency. Female Sprague-Dawley rats were assigned to control, OVX, OVX + vehicle, OVX + empagliflozin (10 mg/kg/day), and OVX + estradiol (20 µg/kg/day) groups for 28 days. Vascular reactivity was assessed using wire myography, alongside evaluation of endothelial nitric oxide synthase (eNOS) expression and nitric oxide (NO) levels. OVX rats exhibited impaired endothelium-dependent vasorelaxation, increased vasoconstriction, reduced eNOS activation, and decreased NO bioavailability. Empagliflozin significantly improved vascular reactivity, enhanced eNOS activation, and restored NO levels, with effects comparable to estradiol. These findings identify empagliflozin as a potential non-hormonal therapeutic strategy for endothelial dysfunction in postmenopausal conditions.
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