Abstract
We investigated the effect of Yi Gong San (YGS) decoction on iron homeostasis and the possible underlying mechanisms in a mouse model of acute inflammation in this study. Our findings suggest that YGS regulates iron homeostasis by downregulating the level of HAMP mRNA, which may depend on regulation of the IL-6/STAT3 or BMP/HJV/SMAD pathway during acute inflammation.
Highlights
Iron plays a pivotal role in cell survival and proliferation
The bone morphogenic protein (BMP)/hemojuvelin (HJV)/SMAD pathway is the major regulator of hepcidin expression that responds to iron status
Metabolic iron homeostasis is regulated by several factors but is most closely related to hepcidin, the central mediator of iron homeostasis
Summary
Iron plays a pivotal role in cell survival and proliferation. It is an important source of nutrition in the competition between microbial pathogens and their hosts [1]. Increased production of inflammatory cytokines can directly induce changes in iron homeostasis, which are characterized by reduction of both iron absorption and macrophage iron release. Hepcidin impairs iron absorption and macrophage iron release and acts as a major hormonal regulator of iron homeostasis [1, 3]. The bone morphogenic protein (BMP)/hemojuvelin (HJV)/SMAD pathway is the major regulator of hepcidin expression that responds to iron status. The expression of hepcidin in isolated primary hepatocytes increases in response to infection/inflammation stimulated by IL6, IL-1, and LPS [5]. We investigated iron homeostasis in a mouse model of LPS-induced acute inflammation
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