Abstract
Acute inflammation is a protective response of the host to physical injury and invading infection. Timely treatment of acute inflammatory reactions is essential to prevent damage to organisms that can eventually lead to chronic inflammation. Forsythoside A (FTA), an active constituent of Forsythia suspensa, has been reported to have anti-inflammatory, antioxidant, and antibacterial properties. Despite increasing knowledge of its anti-inflammatory effects, the mechanism and the effects on acute inflammation are poorly understood. This study is aimed at exploring the pro-resolving effects of FTA on zymosan-induced acute peritonitis. FTA significantly alleviated peritonitis as evidenced by the decreased number of neutrophils and levels of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1) in the peritoneal cavity, without interfering with interleukin-10 (IL-10). FTA showed marked regulation of inflammatory cytokines and chemokine levels in zymosan-stimulated RAW 264.7 macrophages. Moreover, FTA could suppress the activation of NF-κB. In conclusion, FTA alleviated zymosan-induced acute peritonitis through inhibition of NF-κB activation.
Highlights
Inflammation can usually be divided into two major categories according to the course of disease: acute inflammation and chronic inflammation
Burns, wounds, infections, and other conditions would lead to acute inflammation, resulting in the release of a large number of inflammatory factors, which would cause systemic inflammatory response syndrome (SIRS), which could further develop into multiple organ dysfunction syndrome (MODS), eventually causing death [1,2,3]
To evaluate the inflammation-resolution of an acute peritonitis model was established in male C57BL/6J mice
Summary
Inflammation can usually be divided into two major categories according to the course of disease: acute inflammation and chronic inflammation. Acute inflammation of abrupt onset, short duration, with exudative lesions is characterized by granulocyte infiltration of inflammatory cells. Burns, wounds, infections, and other conditions would lead to acute inflammation, resulting in the release of a large number of inflammatory factors, which would cause systemic inflammatory response syndrome (SIRS), which could further develop into multiple organ dysfunction syndrome (MODS), eventually causing death [1,2,3]. In response to injury or infection, polymorphonuclear neutrophil (PMN) and eosinophil migrate to inflammatory sites to neutralize and eliminate potentially injurious stimuli. Accompanied by the rapid proliferation of PMN and inflammatory cell infiltration, is the peak of inflammation in the sequence of events, which makes the exit routes available to PMN, including cell clearance and monocyte-derived macrophages.
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