Aim: To investigate the influence of esculentoside A (EsA) on autoimmunity in mice and its possible mechanisms.
Methods: The level of anti-ds DNA antibody, proliferation of lymphoid cells, and inflammation by pathologic section of joint in mice were examined. The autoimmunity model is made through immunizing mice with formaldehyde treated Campylobacter jejuni strain CJ-S131 and Freund's complete adjuvant. The apoptosis of T cell was analyzed through morphology and flow cytometry (FACS). The expression of ICAM-1 mRNA in human umbilical vein endothelial cell line (ECV304) was determined by coupled reverse transcription and PCR amplification (RT-PCR).
Results: EsA could potently lower the level of anti-ds DNA antibody, inhibit the proliferation of lymphoid cells, and ameliorate inflammation in the joint of model mouse. The apoptosis of thymocyte activated by ConA was markedly accelerated while the expression of ICAM-1 mRNA in ECV304 was decreased by EsA.
Conclusion: EsA has the positive curative effect on autoimmunity in a mouse model, which may function through inhibition of expression of ICAM-1 mRNA in ECV304 and acceleration of thymocyte apoptosis.