Hydroxysafflor yellow A up-regulates HIF-1alpha via inhibition of VHL and p53 in Eahy 926 cell line exposed to hypoxia.
- Author:
Ze-Qin LIAN
1
;
Da-Long ZHAO
;
Hai-Bo ZHU
Author Information
1. Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicines, Ministry of Education, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
- Publication Type:Journal Article
- MeSH:
Carthamus tinctorius;
chemistry;
Cell Hypoxia;
Cell Line;
Cell Proliferation;
drug effects;
Chalcone;
analogs & derivatives;
isolation & purification;
pharmacology;
Endothelial Cells;
cytology;
metabolism;
Flowers;
chemistry;
Humans;
Hypoxia-Inducible Factor 1, alpha Subunit;
biosynthesis;
genetics;
Plants, Medicinal;
chemistry;
Quinones;
isolation & purification;
pharmacology;
RNA, Messenger;
metabolism;
Tumor Suppressor Protein p53;
biosynthesis;
genetics;
Umbilical Veins;
cytology;
Up-Regulation;
Von Hippel-Lindau Tumor Suppressor Protein;
biosynthesis;
genetics
- From:
Acta Pharmaceutica Sinica
2008;43(5):484-489
- CountryChina
- Language:Chinese
-
Abstract:
In present study, we investigated the mechanism of regulating HIF-1alpha expression by hydroxysafflor yellow A (HSYA) in Eahy 926 cell line under 1% O2 hypoxia. Eahy 926 cells were incubated with HSYA (100, 10 and 1 micromol x L(-1)) under hypoxia for the indicated time after treatment. Cell proliferation rate was detected using MTT assays. VHL and p53 location and protein expression were analyzed by immunocytochemical stain. HIF-1alpha, VHL and p53 mRNA expression were detected by RT-PCR. Protein expression of HIF-1alpha, VHL and p53 were assayed by Western blotting method. HSYA at 100 micromol x L(-1) increased Eahy 926 cells proliferation rate under hypoxia. HIF-1alpha mRNA and protein expression were up-regulated in the presence of HSYA. VHL, p53 mRNA and protein expression decreased significantly after 8 hours of treatment under hypoxia. HSYA protected Eahy 926 cells from hypoxia, and up-regulated HIF-1alpha expression partially via its inhibition of VHL and p53 expression.
