Exploring the Anti-Inflammatory Potential of Isoembigenin: A Flavonoid Glycoside from Piper aduncum L. — A Case Exploration through In Vitro , In Vivo , and In Silico Models
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Piper aduncum L. has long been used in traditional medicine for its notable antimicrobial, antidiarrheal, and anti-inflammatory properties. Flavonoids are recognized as the principal bioactive constituents of this plant, among which isoembigenin (IEGN) has been shown to inhibit dendritic cell–mediated inflammatory responses. However, its effects on other immune cell types involved in inflammation remain unclear. In this study, we examined whether IEGN pre-treatment could attenuate macrophage activation triggered by lipopolysaccharide (LPS). Our results demonstrated that IEGN significantly suppressed TNF-α expression in RAW 264.7 macrophages upon LPS stimulation. Moreover, in a murine sepsis model, IEGN pre-treatment markedly reduced the production of proinflammatory cytokines, including TNF-α and IL-1β, shortly after LPS challenge. Importantly, IEGN administration substantially improved the survival rate of BALB/c mice subjected to endotoxininduced shock. Finally, the molecular docking simulation was a hypothetical assessment of the interaction between IEGN and iNOS and COX-2. Taken together, these findings highlight the therapeutic potential of IEGN as a candidate for preventing inflammation driven by macrophage activation.
Abstract
Piper aduncum L. has long been used in traditional medicine for its notable antimicrobial, antidiarrheal, and anti-inflammatory properties. Flavonoids are recognized as the principal bioactive constituents of this plant, among which isoembigenin (IEGN) has been shown to inhibit dendritic cell–mediated inflammatory responses. However, its effects on other immune cell types involved in inflammation remain unclear. In this study, we examined whether IEGN pre-treatment could attenuate macrophage activation triggered by lipopolysaccharide (LPS). Our results demonstrated that IEGN significantly suppressed TNF-α expression in RAW 264.7 macrophages upon LPS stimulation. Moreover, in a murine sepsis model, IEGN pre-treatment markedly reduced the production of proinflammatory cytokines, including TNF-α and IL-1β, shortly after LPS challenge. Importantly, IEGN administration substantially improved the survival rate of BALB/c mice subjected to endotoxininduced shock. Finally, the molecular docking simulation was a hypothetical assessment of the interaction between IEGN and iNOS and COX-2. Taken together, these findings highlight the therapeutic potential of IEGN as a candidate for preventing inflammation driven by macrophage activation.