The phytochemical, EGCG, extends lifespan by reducing liver and kidney function damage and improving age-associated inflammation and oxidative stress in healthy rats
The phytochemical, EGCG, extends lifespan by reducing liver and kidney function damage and improving age-associated inflammation and oxidative stress in healthy rats
复制标题
植物化学物质 EGCG 通过减少健康大鼠的肝肾功能损伤并改善与年龄相关的炎症和氧化应激来延长寿命。
DOI:
10.1111/acel.12133
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发表时间:
2013-12-01
期刊:
影响因子:
7.8
通讯作者:
Sun, Changhao
中科院分区:
文献类型:
--
作者:
Niu, Yucun;Na, Lixin;Sun, Changhao
It is known that phytochemicals have many potential health benefits in humans. The aim of this study was to investigate the effects of long-term consumption of the phytochemical, epigallocatechin gallate (EGCG), on body growth, disease protection, and lifespan in healthy rats. 68 male weaning Wistar rats were randomly divided into the control and EGCG groups. Variables influencing lifespan such as blood pressure, serum glucose and lipids, inflammation, and oxidative stress were dynamically determined from weaning to death. The median lifespan of controls was 92.5weeks. EGCG increased median lifespan to 105.0weeks and delayed death by approximately 8-12weeks. Blood pressure and serum glucose and lipids significantly increased with age in both groups compared with the levels at 0week. However, there were no differences in these variables between the two groups during the whole lifespan. Inflammation and oxidative stress significantly increased with age in both groups compared with 0week and were significantly lower in serum and liver and kidney tissues in the EGCG group. Damage to liver and kidney function was significantly alleviated in the EGCG group. In addition, EGCG decreased the mRNA and protein expressions of transcription factor NF-B and increased the upstream protein expressions of silent mating type information regulation two homolog one (SIRT1) and forkhead box class O 3a (FOXO3a). In conclusion, EGCG extends lifespan in healthy rats by reducing liver and kidney damage and improving age-associated inflammation and oxidative stress through the inhibition of NF-B signaling by activating the longevity factors FoxO3a and SIRT1.