Experimental study on effect of epimedium flavonoids in protecting telomere length of senescence cells HU.
- Author:
Zuo-Wei HU
1
;
Zi-Yin SHEN
;
Jian-Hua HUANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cells, Cultured; Cellular Senescence; genetics; Cyclin-Dependent Kinase Inhibitor p16; biosynthesis; genetics; Epimedium; chemistry; Fibroblasts; cytology; Flavonoids; pharmacology; Male; RNA, Messenger; biosynthesis; genetics; Rats; Rats, Sprague-Dawley; Retinoblastoma Protein; metabolism; Telomerase; biosynthesis; Telomere; genetics; metabolism; Transduction, Genetic
- From: Chinese Journal of Integrated Traditional and Western Medicine 2004;24(12):1094-1097
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the mechanism of senescence delay of human diploid fibroblast (2BS) and protecting telomere length by epimedium flavonoids (EF).
METHODSThe drug sera of EF were used to treat the 2BS. The population doublings of 2BS cells were observed, the mRNA expression of p16 gene were determined by fluorescence real-time quantitative RT-PCR, the telomerase activation of 2BS cells were determined by TRAP-Hyb, the total retinoblastoma (Rb) and phosphorated Rb protein content were detected by ELISA, the telomere length of 2BS cells were determined by telomere restriction fragment (TRF) Southern blot assay.
RESULTSEF could significantly extend the population doublings of 2BS cells, the expression of p16 mRNA was decreased and the content of phosphorated Rb protein were increased by EF. The telomere lengthening of 2BS cells were improved by EF, but the telomerase was not activated.
CONCLUSIONIn senescence human fibroblasts 2BS cells, p16 gene mRNA expression increased, content of phosphorated Rb protein decreased and the telomere length of 2BS shortened, EF might delay the aging of cells through inhibiting the p16 gene expression, promoting the production of phosphorated Rb protein and to protect the length of telomere, but not activating the telomerase.