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Quercetin prevents LPS-induced high-mobility group box 1 release and proinflammatory function
Daolin Tang1, Rui Kang, Weimin Xiao
1Laboratory of Shock, Department of Pathophysiology, Xiangya School of Medicine, Changsha, Hunan, People's Republic of China.
Summary
Quercetin, an experimental therapeutic, reduces lethal systemic inflammation in endotoxemia by inhibiting the release and activity of high-mobility group box 1 (HMGB1) protein. This suggests quercetin
Area of Science:
- Biochemistry
- Immunology
- Pharmacology
Background:
- Sepsis pathogenesis involves pathogen-associated molecular patterns like bacterial endotoxin.
- High-mobility group box 1 (HMGB1) is a late-acting proinflammatory mediator in lethal sepsis.
- Quercetin shows protective effects against oxidative injury.
Purpose of the Study:
- To investigate quercetin's therapeutic potential in endotoxemia.
- To determine if quercetin attenuates systemic inflammation by targeting HMGB1.
- To explore the mechanisms underlying quercetin's anti-inflammatory effects.
Main Methods:
- Administered quercetin to animals with established endotoxemia.
- Measured circulating HMGB1 levels.
- Assessed HMGB1 release and activity in macrophage cultures.
- Analyzed signaling pathways (MAPK, NF-kappaB) and autophagy markers (LC3).
Main Results:
- Quercetin treatment significantly reduced lethal systemic inflammation and circulating HMGB1 levels.
- Quercetin inhibited HMGB1 release and its pro-inflammatory cytokine activities in macrophages.
- Quercetin suppressed MAPK and NF-kappaB activation, crucial for HMGB1-induced cytokine release.
- Quercetin interfered with HMGB1 translocation and release, potentially via autophagy pathways.
Conclusions:
- Quercetin is a promising therapeutic strategy for inhibiting HMGB1 release in endotoxemia.
- Quercetin's efficacy, even when initiated after early inflammatory responses, warrants further investigation.
- Quercetin may be a valuable treatment for sepsis and other systemic inflammatory disorders.
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