Key result
Vortioxetine treatment protected against chronic unpredictable mild stress-induced cardiac damage in rats by normalizing histopathological and immunohistochemical changes (p≤0.001).
Why the study?
Although the harmful effects of stress on the heart are widely recognized, cellular-level investigations remain limited, and the potential protective effects of vortioxetine against stress-induced cardiac damage required evaluation.
Does vortioxetine prevent cardiac damage in a rat model of chronic unpredictable mild stress?
Does vortioxetine prevent cardiac damage in a rat model of chronic unpredictable mild stress?
Vortioxetine demonstrates potential protective effects against stress-induced cardiac damage in a rat model, highlighting its possible cardiovascular benefits.
Vortioxetine may attenuate stress-induced cardiac pathology in rats; leaves open translation to human cardiovascular protection.
Background Stress arises in response to threats or challenges, affecting both physical and mental health. While its harmful effects on the heart are widely recognized, cellular-level investigations remain limited. Antidepressants, including vortioxetine (VOR), are known to impact the cardiovascular system. VOR, used to treat major depressive disorder, is considered a promising option for patients with heart disease due to its anti-inflammatory and antioxidant properties, which may reduce cardiac damage. Objectives This study aimed to assess the effects of chronic unpredictable mild stress (CUMS) on rat hearts and evaluate VOR’s potential protective effects against stress-induced cardiac damage. Methods Twenty-eight male Wistar Albino rats were divided into four groups. The CUMS group experienced random daily stress for 6 weeks, while the CUMS+VOR group received VOR treatment alongside stress. VOR and control groups were not exposed to stress. Heart samples were examined histopathologically and immunohistochemically. Results The CUMS group showed increased hyperemia, hemorrhage, edema, vacuolar degeneration, and mononuclear cell infiltrations, with reduced troponin and IL-10 and increased caspase-3 and NF-κB expressions compared to the control group (p≤0.001). VOR treatment improved these findings, normalizing histopathological and immunohistochemical results. Conclusions CUMS caused significant cardiac damage in rats, while VOR treatment showed protective effects by alleviating these pathological changes.
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Özmen et al. (2025) studied Stress-induced cardiac damage (n=28). Vortioxetine vs. Chronic unpredictable mild stress without treatment, and unstressed controls was evaluated on Histopathological and immunohistochemical cardiac changes (p=≤0.001). Vortioxetine treatment protected against chronic unpredictable mild stress-induced cardiac damage in rats by normalizing histopathological and immunohistochemical changes (p≤0.001).
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