Ophiopogonin D attenuates the progression of murine systemic lupus erythematosus by reducing B cell numbers

Abstract

AbstractSystemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by immune abnormalities leading to multi‐organ damage. The activation of autoreactive B cell differentiation will lead to the production of pathogenic autoantibodies, contributing to the development of SLE. However, the effects of Ophiopogonin D (OP‐D) on B cell activation and autoantibody production as well as renal injury in the pathogenesis of SLE remain unclear. MRL/lpr mice, one of the most commonly used animal models of SLE, were intragastrically administered with 5 mg/kg/d OP‐D at 17 weeks of age for 3 weeks. The survival rates of mice in each group were monitored for 6 weeks until 23 weeks of age. Proteinuria and serum creatinine levels were measured. Serum levels of immunoglobulin (Ig)G, IgM, and anti‐dsDNA autoantibodies were detected by enzyme‐linked immunosorbent assay. Numbers of CD19+ B cells in the blood, spleen and bone marrow and numbers of splenic germinal center (GC) B cells were calculated by using flow cytometry. OP‐D treatment prolonged survival in MRL/lpr mice. OP‐D treatment reduced proteinuria and serum creatinine levels as well as mitigated renal pathological alternation in MRL/lpr mice. Furthermore, serum levels of IgG, IgM, and anti‐dsDNA autoantibodies were reduced by OP‐D treatment. OP‐D lessened not only CD19+ B cells in the spleen and bone marrow but also plasma cells that secreted anti‐dsDNA autoantibodies, IgG and IgM in the spleen and bone marrow. OP‐D ameliorated the progression of SLE by inhibiting the secretion of autoantibodies though reducing B cell numbers.