【摘要】 目的 :探讨补肾复方下调老年大鼠T细胞凋亡的分子机理。方法 :采用RNA酶保护技术 ,测定各组Fas、FasL基因的mRNA水平 ,并以GAPDH为内对照基因 ,对各组Fas、FasL基因的转录进行半定量分析。结果 :老年对照组Fas/GAPDH、FasL/GAPDH的积分光密度值分别为 0 81± 0 17、0 84± 0 12 ;年轻对照组分别为 0 36± 0 16、0 2 6± 0 12。两组比较差异有显著性。活血复方组Fas/GAPDH、FasL/GAPDH的积分光密度值分别为 0 99± 0 36、0 94± 0 33,与老年对照组比较 ,差异无显著性 (P >0 0 5) ;两个补肾组Fas/GAPDH为 0 78± 0 11和 0 78± 0 2 0 ,与老年对照组比较差异无显著性 (P >0 0 5) ;而两个补肾组FasL/GAPDH的积分光密度值为 0 71± 0 2 1和 0 68± 0 15,低于老年对照组 (P <0 0 1)。结论 :补肾复方对T细胞FasL基因的转录具有一定的负调控作用 ,这是补肾复方下调老年大鼠T细胞过度凋亡的分子机理之一更多还原

【Abstract】 Objective: To probe the molecular mechanism for down regulation of T cell apoptosis by Kidney tonifying compound (KTC) in aged rats. Methods: GAPDH was used as an internal control gene, and semi quantitative analysis of the transcription of Fas and FasL genes was performed by using RNase protection assay. Results: The Fas/GAPDH and FasL/GAPDH optical density (OD) ratios was 0.81±0.17 and 0.84±0.12 in the aged control group, and 0.36±0.16 and 0.26±0.12 in the young control group. the difference between the two groups was significant. In the circulation promoting group, the parameters were 0.99± 0.36 and 0.94±0.33 which were not significantly different as compared with those in the aged control group (P>0 05). In the two Kidney tonifying groups, the Fas/GAPDH OD ratio was 0.78±0.11 and 0.78±0.20, respectively, and no significant difference was observed as compard with those in the aged control group. However the FasL/GAPDH OD ratios in the two kidney tonifying group were 0.71±0.21 and 0.68±0.15 , which were lower than those in the aged control group (P<0 01). Conclusion: The negative regulation of FasL gene expression may be one of the molecular mechanisms of KTC in down regulating excessive apoptosis of T cell in aged rats.更多还原