慢性病贫血（anemia of chronic disease，ACD）是一种铁代谢异常疾病，异功散（YGS）可治疗ACD。研究发现YGS不仅通过IL-6/JAK/STAT通路影响hepcidin-ferroportin轴，调节铁代谢，还调节ActinvinB/SMAD通路关键蛋白。结合“炎症可通过ActinvinB竞争性结合BMP受体，协同IL-6/JAK/STAT对铁代谢的调控”的新认识，提出假说：YGS可通过影响ActinvinB/SMAD对IL-6/JAK/STAT通路的协同作用调节ACD铁代谢。本研究用LPS激活小鼠ActinvinB/SMAD通路，siRNA技术分别沉默HepG2细胞的SMAD1/5/8和STAT3基因，围绕IL-6/JAK/STAT及ActinvinB/SMAD通路的关键环节，从整体动物与体外细胞两层次、正反两方面验证该假说，阐释YGS调节ACD铁代谢的机理。

Anemia of chronic disease (ACD) is a disease of iron metabolism, and YGS can treat ACD. The study found that: YGS not only affects the hepcidin-ferroportin axis through the IL-6/JAK/STAT pathway, regulates iron metabolism, but also regulates the key protein of ActinvinB/SMAD pathway. Combining the new understanding of "inflammation can regulate iron metabolism through Actinvin B competitively bind BMP receptorand to cooperate with IL-6/JAK/STAT ", hypothesis is put forward: YGS can regulates iron metabolism of ACD by synergic effecting of ActinvinB/SMAD on IL-6/JAK/STAT pathway. In this study, LPS was used to activate the ActinvinB/SMAD pathway in mice. The siRNA technology silenced the SMAD1/5/8 and STAT3 genes in HepG2 cells, and the key links of the IL-6/JAK/STAT and ActinvinB/SMAD pathways, from the overall animal and in vitro. The hypothesis was verified in two levels, positive and negative, to elucidate the mechanism by which YGS regulates iron metabolism of ACD.