Abstract
Lipopolysaccharides (LPS) are major components of Gram-negative bacteria. LPS not only induce endotoxemia and inflammation, but also contribute to various diseases. In experimental settings, LPS administration serves as a model for acute inflammatory responses. This study aims to evaluate the anti-inflammatory potential and mechanism of action of palmitoylated prolactin-releasing peptide (palm11-PrRP31) in a rat model of LPS-induced inflammation. Palm11-PrRP31 has demonstrated its efficacy in mitigating LPS-induced weight loss and anorexia, emphasizing its potential protective effects. Cytokine profiles revealed a consistent reduction in tumor necrosis factor α, highlighting the potent anti-inflammatory effects of palm11-PrRP31. The peptide also modulated key cytokines and chemokines in plasma, the liver, and the hypothalamus, reflecting its broad-spectrum anti-inflammatory properties. Palm11-PrRP31 also effectively attenuated the expression levels of TLR4 signaling components in the liver, suggesting its suppressive effects on the activation of these pathways during LPS-induced inflammation. These anti-inflammatory effects were specific to palm11-PrRP31, whereas natural PrRP31 had minimal impact. In conclusion, this study reveals the efficacy of palm11-PrRP31 in modulating LPS-induced inflammation, offering insights into its immunomodulatory properties. The abilities of the peptide to suppress proinflammatory responses and attenuate relevant signaling pathways indicate its potential use as a therapeutic agent for inflammatory disorders.
Published Version
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