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目的 :探讨抗L3T4单克隆抗体对线粒体腺苷酸转移酶 (adeninenucleotidetranslocator ,ANT)多肽诱导的小鼠心肌病是否有治疗作用。方法 :15只雄性Balb/c小鼠分为 3组 :①免疫应答组 (n =5 ) :予ANT多肽免疫诱导心肌病的产生 ;②免疫治疗组 (n =5 ) :先予ANT多肽免疫 ,喂养 3个月后再给予抗L3T4单抗进行治疗 ;③对照组 (n =5 ) :以不含ANT合成肽的空白免疫液免疫小鼠。采用ELISA法检测血清抗ANT多肽抗体动态变化 ,实验结束时在光镜和电镜下观察小鼠心肌组织的病理改变 ,计算组织中的胶原纤维容积分数。实验期半年。结果 :免疫应答组小鼠体内均有ANT抗自身抗体的产生 ,且抗体的光密度值 (A )明显增高 ,与对照组相比差异有统计学意义 (P <0 .0 1) ;免疫治疗组小鼠经抗L3T4单抗治疗后自身抗体出现反应性下降 ,其A值与免疫应答组及对照组比较差异均有统计学意义 (均P <0 .0 1) ;对照组抗体检测为阴性。病理结果显示 ,免疫应答组小鼠心肌组织出现弥漫性纤维化 ,心肌细胞线粒体和肌丝有明显损害 ,心肌胶原纤维容积分数明显高于对照组(P <0 .0 1) ;免疫治疗组小鼠心肌组织的病理改变略轻于免疫应答组 ,心肌胶原纤维容积分数介于免疫应答组和对照组之间 ;对照组心肌组织基本正常。结论 :ANT多肽可诱导小鼠产生抗AN
OBJECTIVE: To investigate whether anti-L3T4 monoclonal antibody has a therapeutic effect on mouse cardiomyopathy induced by adenine nucleotide translocator (ANT) polypeptide. Fifteen male Balb / c mice were divided into three groups: ① immune response group (n = 5): induced cardiomyopathy induced by ANT polypeptide; ② immunotherapy group (n = 5) , 3 months after feeding anti-L3T4 monoclonal antibody treatment; ③ control group (n = 5): immunized mice with blank immunized solution without ANT synthetic peptide. The serum anti-ANT polypeptide antibody was detected by ELISA. At the end of the experiment, the pathological changes of myocardial tissue were observed under light and electron microscopes, and the collagen fiber volume fraction was calculated. Experimental period of six months. Results: The ANT anti-autoantibodies were all produced in the immune response mice, and the antibody optical density value (A) was significantly higher than that in the control group (P <0.01); immunotherapy After anti-L3T4 monoclonal antibody treatment, the autoantibodies in the mice showed decreased reactivity, and the difference was significant between the A value and the immune response group and the control group (all P <0.01); the antibody in the control group was negative . The pathological results showed that there was diffuse fibrosis, myocardial mitochondria and myofilament damage, myocardial collagen fiber volume fraction in the immune response group was significantly higher than that in the control group (P <0.01), immunotherapy group was smaller The pathological changes of myocardial tissue in rats were slightly lighter than those in immune response group. The volume fraction of myocardial collagen fibers was between immune response group and control group. The myocardial tissue in control group was normal. Conclusion: ANT polypeptide can induce anti-AN in mice