黄山药总皂苷对晚期糖基化终产物诱导心肌老化的保护作用及机制  

Protective effect of total saponins of dioscorea pathaica on cardiac senescence induced by advanced glycation end-products and its mechanism

作　　者：徐婉莹 查志敏 冯楚炎 郭妍 XU Wan-Ying;ZHA Zhi-Min;FENG Chu-Yan;GUO Yan(Department of Geriatric Cardiology, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China;Department of Geriatrics, Northern Jiangsu People′s Hospital, Yangzhou 225001, Jiangsu Province, China)

机构地区：[1]南京医科大学第一附属医院老年心血管内科,南京210029 [2]苏北人民医院老年科,江苏扬州225001

出　　处：《中华老年多器官疾病杂志》2020年第7期545-550,共6页Chinese Journal of Multiple Organ Diseases in the Elderly

基　　金：江苏省干部保健科研课题(BJ18017)。

摘　　要：目的研究黄山药总皂苷(TSDP)对晚期糖基化终产物(AGEs)诱导的心肌老化产生的作用并初步探讨其机制。方法用不同浓度TSDP干预原代心肌细胞,以CCK-8试剂盒(CCK-8)检测细胞活性。细胞预先TSDP干预2h后加入AGEs,通过免疫印迹实验检测沉默信息调节因子(SIRT3)、超氧化物歧化酶-2(SOD2)、及衰老相关蛋白p53和p16水平的表达;2′,7′-二氯二氢荧光素二乙酸酯探针(DCFH-DA)检测细胞内活性氧(ROS)。结果与对照组比较,AGEs干预组β半乳糖苷酶(SA-β-Gal)活性增加,p53和p16蛋白水平增加,SOD2和SIRT3蛋白表达下降,ROS产生增多,差异有统计学意义(P<0.05)。与AGEs组相比,TSDP预干预组SA-β-Gal活性降低,SIRT3和SOD2蛋白水平增加,p53和p16下降,ROS增加,差异有统计学意义(P<0.05)。结论TSDP对AGEs诱导的心肌细胞老化起保护作用,其机制可能与升高SIRT3和调节氧化应激有关。Objective To investigate the effect of total saponins of Dioscorea pathaica(TSDP)on cardiac senescence induced by advanced glycation end-products(AGEs)and its mechanism.Methods Neonatal rat cardiomyocytes were incubated with different concentrations of TSDP,and cell viability was measured by Cell Counting Kit-8(CCK-8).AGEs were added 2h after the cells were pre-treated with TSDP.Western blotting was used to detect levels of silent mating type information regulation 2 homolog-3(SIRT3),superoxide dismutase-2(SOD2),and aging-related p53 and p15.2,7-Dichlorodi-hydrofluorescein diacetate(DCFH-DA)was used to detect intracellular reactive oxygen species(ROS).Results Compared with the control group,the activity of SA-β-Gal and the level of p53 and p16 increased,the production of ROS increased,and the expression of SOD2 and SIRT3 decreased in the AGEs group,the differences being statistically significant(P<0.05).Compared with the AGEs group,the activity of SA-β-Gal decreased,ROS increased,SIRT3 and SOD2 protein levels increased,and p53 and p16 decreased in the TSDP pre-treatment group,differences being statistically significant(P<0.05).Conclusion TSDP has protective effects on AGEs-induced cardiomyocyte aging,and its mechanism may be related to the increase of SIRT3 and regulation of oxidative stress.

关 键 词：黄山药总皂苷 晚期糖基化终产物 心肌细胞老化 SIRT3 氧化应激 

分 类 号：R541[医药卫生—心血管疾病]