In mice with obesity, the drug semaglutide is linked to lower levels of certain biological markers that indicate inflammation and oxidative stress in the blood and heart tissue.
Mechanism
Synthesis from 1 study
Semaglutide helps protect the heart in obese mice by calming down a type of immune cell called neutrophils. When these cells are less active, they release fewer harmful signals and chemicals that cause inflammation and damage, which lets the heart recover from the stress of obesity.
Most probable mechanism
Semaglutide tells certain immune cells called neutrophils to stop releasing harmful signals that attract more immune cells and create damaging chemicals. This reduces the number of inflammatory molecules and reactive chemicals in the heart, which helps protect it from damage caused by obesity.
Semaglutide activates GLP-1 receptors on immune cells or alters systemic metabolism in a way that suppresses neutrophil activation
Reduced expression of Cxcl2 in neutrophils decreases chemotactic signaling that recruits additional neutrophils and monocytes to cardiac tissue
Reduced expression of S100a8 and S100a9 in neutrophils diminishes formation of the calprotectin complex, which normally activates TLR4/NF-κB signaling and promotes reactive oxygen species production
Lower neutrophil-derived Cxcl2, S100a8, and S100a9 leads to decreased activation of cardiac macrophages and endothelial cells, reducing release of TNF-α, IL-6, and ROS
Decreased levels of TNF-α, IL-6, ROS, and MDA in serum and cardiac tissue result in reduced oxidative damage and inflammation in the heart
Evidence from Studies
Supporting (1)
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