18-β-Glycyrrhetinic-loaded poly(lactic-co-glycolic) (PLGA) nanoparticles downregulate the expression LPS-induced...

Inflammation is a central pathophysiological feature of numerous chronic diseases. While acute inflammation serves to neutralize and eliminate harmful stimuli such as pathogens and toxins, failure to resolve these stimuli can lead to chronic inflammation, resulting in sustained tissue damage. This causes the dysregulated activation of tissue repair mechanisms, which ultimately results in tissue remodelling: a series of irreversible changes in tissue architecture and function. Chronic tissue remodelling is a hallmark of several diseases, including heart failure, characterized by cardiac remodelling, and chronic respiratory disorders like asthma and chronic obstructive pulmonary disease,whereby airway remodelling impairs respiratory function. Therefore, targeting the molecular mechanisms at the intersection of inflammation and remodelling offers a promising therapeutic approach. In the present study, we demonstrate that 18-β-glycyrrhetinic acid (18-β-gly), encapsulated in poly (lactic-co-glycolic acid) (PLGA) nanoparticles, mitigates the effects of bacterial lipopolysaccharide on the expression of key regulators of inflammation and tissue remodelling (EGF, leptin, IL-22, IL-23, and IL-33), in vitro in RAW264.7 mouse macrophages. Our findings highlight the potential of 18-β-gly PLGA nanoparticles as a multifaceted anti-inflammatory and antioxidant phytoceutical capable of targeting remodelling processes in inflammation-driven diseases. This study establishes a foundation for future in-depth investigations into its application for treating chronic conditions characterized by the simultaneous occurrence of inflammation and pathological tissue remodelling.