OBJECTIVE: To investigate the effects of icariin on apoptosis and the expression of Fas, Fas ligand (FasL), B cell lymphoma (Bcl-2), and Bcl-2-associated X protein (Bax) in CD4＋ T lymphocytes from patients with ankylosing spondylitis. METHODS: Primary cultures of peripheral blood CD4+ T lymphocytes were established and treated with icariin at high, medium, and low doses (0.5, 0.25, and 0.125 mg/mL). Sulfasalazine treated and helthy cells were used as controls. Apoptosis of treated cells was determined by flow cytometry. Reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assays were used to determine the effects of icariin on the expression of Fas, FasL, Bcl-2, and Bax. The activity of caspase 8 and caspase 3 was determined by a colorimetric assay. RESULTS: The mRNA and protein expression of Fas, and activity of caspase 8 and caspase 3 in CD4+ T lymphocytes were increased by icariin (P < 0.05). Conversely, the mRNA and protein expression of Bcl-2 was decreased (P < 0.05). The expression of FasL and Bax were not significantly different between groups. The proapoptotic effects of icariin were dose-dependent. CONCLUSION: Icariin induces the apoptosis of CD4 + T cells from patients with AS comparing to normal control. Therefore, the induction of apoptosis may be the likely mechanism of action of icariin's antirheumatics activities.
OBJECTIVE: To investigate the effects of icariin on apoptosis and the expression of Fas, Fas ligand (FasL), B cell lymphoma (Bcl-2), and Bcl-2-associated X protein (Bax) in CD4＋ T lymphocytes from patients with ankylosing spondylitis. METHODS: Primary cultures of peripheral blood CD4+ T lymphocytes were established and treated with icariin at high, medium, and low doses (0.5, 0.25, and 0.125 mg/mL). Sulfasalazine treated and helthy cells were used as controls. Apoptosis of treated cells was determined by flow cytometry. Reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assays were used to determine the effects of icariin on the expression of Fas, FasL, Bcl-2, and Bax. The activity of caspase 8 and caspase 3 was determined by a colorimetric assay. RESULTS: The mRNA and protein expression of Fas, and activity of caspase 8 and caspase 3 in CD4+ T lymphocytes were increased by icariin (P < 0.05). Conversely, the mRNA and protein expression of Bcl-2 was decreased (P < 0.05). The expression of FasL and Bax were not significantly different between groups. The proapoptotic effects of icariin were dose-dependent. CONCLUSION:Icariin induces the apoptosis of CD4 + T cells from patients with AS comparing to normal control. Therefore, the induction of apoptosis may be the likely mechanism of action of icariin's antirheumatics activities.