Semaglutide attenuates excessive exercise-induced myocardial injury through inhibiting oxidative stress and inflammation in rats

Semaglutide significantly increased the survival rate of cardiomyocytes in lipopolysaccharide-treated cells.

• In LPS-treated H9c2 cells, semaglutide reduced cell death and improved cell survival.
• The treatment activated the AMPK pathway, which enhances cellular processes like autophagy.
• Semaglutide decreased the production of reactive oxygen species in these cells.
• In a rat model, chronic semaglutide treatment led to notable increases in myocardial injury markers.
• Pathological analysis demonstrated that semaglutide improved heart tissue structure and reduced lipid accumulation.
• The treatment also lowered levels of inflammation-related proteins such as NF-κB, TNF-α, and IL-1β.

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