Previous studies have shown that sitosterol and β-sitosterol inhibited the activation of TLR4 and NF-kB pathways and reduced the expression of inflammatory factors such as IL-1β, TNF-α, and IL-6.[57,58] Despite our study reveals that the therapeutic mechanism of SGC for HF may be to reduce the overexpression of inflammation by modulating the expression of cytokines such as IL-1β, thereby improving the dysfunction of the heart, there are several limitations. This evidence concerns the gene TLR4 and hydrops fetalis.