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研究老年肾虚T细胞功能减退的机制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制 ,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。
To study the mechanism of aging T-cell dysfunction in the elderly and the immunological basis of kidney-defying anti-aging. Methods Apoptosis of T cells induced by anti-CD3 monoclonal antibody activation 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. The percentage of apoptotic T cells in the blood-activating group was 43.3%, which was not significantly different from the elderly group. Conclusion Activation-induced excessive T cell apoptosis is an important mechanism of aging kidney deficiency T cell dysfunction, and down-regulation of activation-induced T cell apoptosis may be the main way to delay kidney aging immune aging.