Objective:To study the immunologic mechanism of ulcerative colitis (UC) and the treatment mechanism of Chang Yan Kang (CYK).
Methods:The UC rat models are reproduced successfully by immune method. CYK and Salicylazosulfapyridine (SASP) were applied to the models for 50 days. Some changes before and after treatment including the levels of
spleen cell ConA SI,LPS SI,IL 2,IFN r, NKc killing activating in model rats were analyzed. Results:Compared with normal group, spleen cell Con SI, NKc killing activity ( P <0.01) and IL 2,IFN r level decreased significantly in model group ( P <0.05) and
spleen cell LPS SI increased ( P <0.05). Spleen cell ConA SI, IL 2,IFN r level and NKc killing activity after treatment increased significantly in CYK group, but no significant difference in spleen cell LPS SI compared with model group ( P >0.05). Spleen cell LPS SI( P <0.05) decreased significantly in SASP group and spleen cell ConA increased ( P <0.05),but which was lower than that in CYK group( P <0.05).There was no significant difference in IL 2,IFN r level and NKc killing activity ( P <0.05) compared with model group, which was lower than normal group ( P <0.05). Conclusion:The results show a decrease in cellular immunity, NKc killing activity and increase in humoral immunity of UC rats. CYK can help the restoration of colonic mucosa of UC rats and disappearance of inflammation. It is superior to SASP in increasing NKc killing activity and restoring the cellular immunity of UC rats, but less effective in inhibiting humoral immunity in UC rats.