ABSTRACT
ObjectiveThe aim of this study is to investigate whether oral administration of collagen Ⅱ peptide (250-270)[C Ⅱ (250-270)]-cholera toxin B subunit (CTB)complex could effectively set up oral immune tolerance to collagen-induced arthritis (CIA) in mice. MethodsDBA/1 mice were divided into Ⅰ, Ⅱ, Ⅲ and Ⅳgroups. Group Ⅰ was normal control group. Collagen type Ⅱ emulsified in Freund's complete adjuvant were injected to mice of groups Ⅱ , Ⅲ and Ⅳ twice from the base of the tail. Mice of group Ⅲ were fed with C Ⅱ (250-270)-CTB covalent complex twice after the arthritis was developed. Mice of group Ⅳ were fed with C Ⅱ(250-270) and CTB mix at the 14th day after primary immunization. Visual scores and histopathologic scores of arthritis were recorded. The frequencies of arthritis between the groups were compared usingFisher's exact test. The clinical and histological severity of arthritis were analyzed by ANOVA.Results The frequencies of arthritis in groups Ⅰ , Ⅱ , Ⅲ and Ⅳ were 0, 100％, 100％ and 25％ respectively. Average accumulative scores of arthritis were 0, 5.0±1.7, 10.8±2.8 and 1.0±2.0 respectively. Average accum-ulative histopathological scores of arthritis were 0, 16±8, 32±13 and 7±6 respectively. Conclusion Oral administration of C Ⅱ (250-270) and CTB mix in arthritis mice after C Ⅱ immunization can suppress the onset and severity of arthritis. Oral administration of C Ⅱ (250-270)-CTB covalent complex in the acute stage of arthritis can accelerate arthritis.
ABSTRACT
Objective:To study the effects of dexamethasone(DEX)on the cytotoxicity and apoptosis of NK-92MI cells and the mechanisms involved.Methods:NK-92MI cells were treated with different doses of DEX.The proliferative rate and cytotoxicity of the NK-92MI cells were detected by MTT colorimetry.The cell apoptotic rate was observed by flow cytometry with Annexin V and propidium iodide(PI)double staining.The expression of apoptosis-related gene,Bcl-2 and Bax was detected by RT-PCR.Results:After treated with 1?10-8mol/L to 1?10-3mol/L of DEX for 24 h,48 h and 72 h,the proliferation of NK-92MI cells was significant inhibited(P