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Background <p>Although the various pharmacological activities of albiflorin, a monoterpene glycoside, are closely related to its anti-inflammatory and antioxidant activities, studies on these activities in macrophages are limited.</p> Objectives <p>This study aimed to investigate whether albiflorin, through its anti-inflammatory activity, can mitigate oxidative stress in a lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage model.</p> Results <p>Albiflorin substantially reduced the production of pro-inflammatory cytokines interleukin (IL)-6, IL-1β, and tumor necrosis factor-α by lowering their expression. Albiflorin also significantly decreased the secretion of inflammatory mediators such as nitric oxide (NO) and prostaglandin E₂ by downregulating the expression of inducible NO synthase and cyclooxygenase-2 in LPS-stimulated RAW 264.7 cells. Moreover, albiflorin impeded the LPS-induced phosphorylation of mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB). In terms of antioxidant activity, albiflorin significantly decreased LPS-induced reactive oxygen species levels while enhancing heme oxygenase-1 (HO-1) expression and promoting nuclear factor erythroid 2-related factor 2 (Nrf2) activation, suggesting that albiflorin activates the Nrf2/HO-1 pathway. Importantly, the anti-inflammatory effects of albiflorin were reversed by zinc protoporphyrin, a selective HO-1 inhibitor, confirming the critical role of the Nrf2/HO-1 pathway in mediating albiflorin bioactivity.</p> Conclusion <p>These findings indicate that albiflorin exhibits anti-inflammatory and antioxidant properties in an in vitro model, likely mediated through the regulation of the MAPK/NF-κB and Nrf2/HO-1 pathways. These results provide preliminary mechanistic insight and support the need for further investigation to determine its potential relevance in vivo.</p>

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Albiflorin reduces lipopolysaccharide-induced inflammatory responses and oxidative stress by regulating the NF-κB and Nrf2/HO-1 signaling pathways in RAW 264.7 macrophages

  • 期刊论文

  • 发表日期：

    2026年5月10日

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  • Yung Hyun Choi

摘要

Background

Although the various pharmacological activities of albiflorin, a monoterpene glycoside, are closely related to its anti-inflammatory and antioxidant activities, studies on these activities in macrophages are limited.

Objectives

This study aimed to investigate whether albiflorin, through its anti-inflammatory activity, can mitigate oxidative stress in a lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage model.

Results

Albiflorin substantially reduced the production of pro-inflammatory cytokines interleukin (IL)-6, IL-1β, and tumor necrosis factor-α by lowering their expression. Albiflorin also significantly decreased the secretion of inflammatory mediators such as nitric oxide (NO) and prostaglandin E₂ by downregulating the expression of inducible NO synthase and cyclooxygenase-2 in LPS-stimulated RAW 264.7 cells. Moreover, albiflorin impeded the LPS-induced phosphorylation of mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB). In terms of antioxidant activity, albiflorin significantly decreased LPS-induced reactive oxygen species levels while enhancing heme oxygenase-1 (HO-1) expression and promoting nuclear factor erythroid 2-related factor 2 (Nrf2) activation, suggesting that albiflorin activates the Nrf2/HO-1 pathway. Importantly, the anti-inflammatory effects of albiflorin were reversed by zinc protoporphyrin, a selective HO-1 inhibitor, confirming the critical role of the Nrf2/HO-1 pathway in mediating albiflorin bioactivity.

Conclusion

These findings indicate that albiflorin exhibits anti-inflammatory and antioxidant properties in an in vitro model, likely mediated through the regulation of the MAPK/NF-κB and Nrf2/HO-1 pathways. These results provide preliminary mechanistic insight and support the need for further investigation to determine its potential relevance in vivo.