Baicalin inhibits IgG production by regulating Treg/Th17 axis in a mouse model of red blood cell transfusion.

This study was conducted to evaluate whether baicalin inhibits red blood cell (RBC) immunization and elucidate the underlying mechanism. We used human RBCs with adjuvant lipopolysaccharide (LPS) and transfused mice to induce antibodies as an experimental system for studying the effect of baicalin on RBC immunization. Mice were divided into a human RBC transfused positive control group administered with human RBC and LPS intravenously once or weekly for 4 weeks, control group administered dexamethasone (DEX) intraperitoneally daily for 4 weeks, and treatment group administered baicalin intraperitoneally daily for 4 weeks. Assessment of human RBC immunization was performed by measuring serum immunoglobulin G (IgG) and immunoglobulin M (IgM) against human RBC weekly. Lymphocyte changes in spleen were monitored by flow cytometry. We found that baicalin treatment significantly decreased serum IgG but not IgM production in a time and does dependent manner, with a concomitant reduction in Th17 cells and increase in CD4 regulatory T cells in the spleen. The percentage of CD4-positive cells in the spleen was not decreased in the baicalin-treated group but was decreased in the dexamethasone-treated group. In conclusion, baicalin inhibited RBC immunization, particularly IgG production by regulating the Treg/Th17 axis without damaging spleen function.