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目的 :研究老年肾虚T细胞功能减退的机理以及补肾延缓衰老的免疫学基础。方法 :采用电镜、DNA凝胶电泳及TUNEL标记的流式细胞检测技术 ,对各组大鼠抗CD3单抗激活诱导的T细胞凋亡进行定性、定量分析。结果 :老年组激活诱导的T细胞凋亡百分率为 47 0 % ,年轻组为 2 2 2 % (P <0 0 1) ;补肾组为 31 2 % ,明显低于老年组 (P <0 0 5 ) ;活血组T细胞凋亡百分率为 43 3% ,与老年组比较无显著性差异。结论 :激活诱导的T细胞过多凋亡是老年肾虚T细胞功能减退的重要机理 ,下调激活诱导的T细胞凋亡可能是补肾延缓免疫衰老的主要途径。
Objective: To study the mechanism of aging T-cell dysfunction in the elderly and the immunological basis of kidney-defying anti-aging. METHODS: The apoptosis-induced T cell apoptosis induced by anti-CD3 monoclonal antibody in each group was qualitatively and quantitatively analyzed by flow cytometry using electron microscopy, DNA gel electrophoresis and TUNEL labeling. Results: The percentage of apoptotic cells induced by activation in the elderly group was 47.0%, in the young group was 22.2% (P <0 01), and in the kidney-tonifying group was 31 2%, which was significantly lower than that in the old group (P <0 0 5 The percentage of apoptotic T cells in the blood-activating group was 43 3%, which was not significantly different from that in the elderly group. Conclusion : Activation-induced excessive apoptosis of T cells is an important mechanism of aging kidney deficiency T cell dysfunction. Down-regulation of activation-induced T cell apoptosis may be the main way to delay kidney aging immune aging.