Related Experiment Video
Updated: Jun 2, 2026
Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes
Published on: May 31, 2018
Dehydrocorydaline inhibits elevated mitochondrial membrane potential in lipopolysaccharide-stimulated macrophages
Kazuhiro Ishiguro1, Takafumi Ando, Osamu Maeda
1Department of Advanced Research of Gastroenterology, Nagoya University Graduate School of Medicine, Tsurumai-cho 65, Showa-ku, Nagoya, Aichi, 466-8550, Japan. kio@med.nagoya-u.ac.jp
Abstract:
Activated macrophages play a critical role in the pathogenesis of numerous diseases by producing pro-inflammatory cytokines such as interleukin (IL)-1β and IL-6. While the mechanisms of bacterial component recognition and signal transduction have been well investigated, viability regulation in activated macrophages remains unclear. We screened herbal ingredients to find an agent that reduces the viability of lipopolysaccharide (LPS)-stimulated macrophages and observed that dehydrocorydaline, a component of Corydalis yanhusuo, reduced the viability of macrophage-derived RAW264.7 cells and primary macrophages in the presence of LPS. Dehydrocorydaline inhibited the elevation of mitochondrial membrane potential and induced ATP depletion in LPS-stimulated macrophages but neither affected basal mitochondrial membrane potential nor ATP content in non-stimulated macrophages. Dehydrocorydaline also prevented increased concentrations of IL-1β and IL-6 in culture media of LPS-stimulated macrophages. Mode of dehydrocorydaline action indicates that elevated mitochondrial membrane potential may be a novel target to specifically reduce viability and suppress cytokine production in LPS-stimulated macrophages.
Insights
Dehydrocorydaline, from Corydalis yanhusuo, reduces the viability of activated macrophages by disrupting mitochondrial function and lowering pro-inflammatory cytokine levels. This suggests targeting mitochondrial membrane potential in inflammatory diseases.
Area of Science:
- Immunology
- Pharmacology
- Cell Biology
Background:
- Activated macrophages are key players in disease pathogenesis, releasing pro-inflammatory cytokines like IL-1β and IL-6.
- Mechanisms of macrophage activation are known, but how their viability is regulated remains unclear.
Purpose of the Study:
- To identify herbal agents that decrease the viability of lipopolysaccharide (LPS)-stimulated macrophages.
- To investigate the mechanism by which dehydrocorydaline affects activated macrophage viability and cytokine production.
Main Methods:
- Screening of herbal ingredients for effects on LPS-stimulated macrophages.
- Assessing dehydrocorydaline's impact on macrophage viability, mitochondrial membrane potential, and ATP levels.
- Measuring IL-1β and IL-6 concentrations in cell culture media.
Main Results:
- Dehydrocorydaline significantly reduced the viability of LPS-stimulated RAW264.7 cells and primary macrophages.
- It inhibited the LPS-induced increase in mitochondrial membrane potential and caused ATP depletion.
- Dehydrocorydaline suppressed the release of IL-1β and IL-6 in LPS-stimulated macrophages.
Conclusions:
- Dehydrocorydaline effectively reduces activated macrophage viability and pro-inflammatory cytokine production.
- Elevated mitochondrial membrane potential in LPS-stimulated macrophages is a potential therapeutic target.
- Dehydrocorydaline's mechanism involves targeting mitochondrial function, offering a novel approach for inflammatory diseases.
