The results showed that the binding ability of ERβ on the OXTR promoter was significantly decreased in the HG(4d) + LG(4d)/CTL group compared to the LG(4d) + LG(4d)/CTL group, and this effect was completely restored by infection of SOD2 in HG(4d) + LG(4d)/↑SOD2 group; on the other hand, other transcription factors, including ERα, showed no significant difference (see Figure 2E), indicating that ERβ is responsible for hyperglycemia-induced OXTR suppression. The gene discussed is SOD2; the disease is infection.