Current research in pharmacology and drug discovery · 2025
MAO-B inhibition by selegiline blunts cardiac functions improved by high-fat diet: Role of inflammation, apoptosis, and calcium-handling.
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Hambalkó Szabolcs, Pelyhe Csilla, Kovácsházi Csenger, Kenyeres Bence, Kiss Bernadett, Ágg Bence, Gergely Tamás G, Weber Bennet Y, Makkos András, Brenner Gábor B, Komlódi Tímea, Tretter László, Horváth Csaba, Jarabicová Izabela, Adameová Adriana, Görbe Anikó, Poggi Paola, Chatgilialoglu Alexandros, Horváth Ildikó, Máthé Domokos, Szigeti Krisztián, Oláh Attila, Radovits Tamás, Varga Zoltán V, Merkely Béla, Baxter Gary F, Schulz Rainer, Ferdinandy Péter, Giricz Zoltán
Аннотация
BACKGROUND: Obesity is a major risk factor for the development of cardiovascular disease. However, recent research shows that moderate obesity reduces the risk of developing cardiovascular disease. We evidenced before that MAO-B inhibitor selegiline reduced visceral adiposity.
AIM: Therefore, our aim was to investigate cardiac effects of selegiline in moderate obesity in rats treated with a high-fat diet (HFD).
KEY FINDINGS: We demonstrated that HFD improved cardiac contractility parameters, which were reversed by selegiline. Enhanced contractility might be attributed to an increased sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA2a) expression and phospholamban pentamerization. Selegiline reduced SERCA2a expression in HFD. HFD increased Tumor necrosis factor and Nuclear factor-kappa B expression which were not affected by selegiline. HFD induced proapoptotic processes, which were restored by selegiline.
CONCLUSION: In conclusion, moderate obesity improves cardiac function through Ca2+ homeostasis and inflammatory processes and MAO-B inhibition reverses these effects.
AIM: Therefore, our aim was to investigate cardiac effects of selegiline in moderate obesity in rats treated with a high-fat diet (HFD).
KEY FINDINGS: We demonstrated that HFD improved cardiac contractility parameters, which were reversed by selegiline. Enhanced contractility might be attributed to an increased sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA2a) expression and phospholamban pentamerization. Selegiline reduced SERCA2a expression in HFD. HFD increased Tumor necrosis factor and Nuclear factor-kappa B expression which were not affected by selegiline. HFD induced proapoptotic processes, which were restored by selegiline.
CONCLUSION: In conclusion, moderate obesity improves cardiac function through Ca2+ homeostasis and inflammatory processes and MAO-B inhibition reverses these effects.