In summary, this study provided strong evidence of the protective effects of AS IV against LPS-induced endometritis in mice, the mechanisms of which could be deduced as involving AS IV inhibiting the LPS-induced production of IL-1β and TNF-α, the concentration of NO, and MPO activity in uteri through the suppressing of TLR4 mediated NF-κB, p38, and JNK signaling pathways (Figure 10). The gene discussed is TLR4; the disease is endometritis.