Effects of naoyian serum on VEGF protein expression in cultured rat cerebral microvascular endothelial cell with hypoxia.
- Author:
Sai-ying WAN
1
;
Xing-qun LI
;
Qin-hua LIANG
;
Yi-hui ZHI
;
Yun LUO
;
Hua-xian ZHANG
Author Information
1. Department of Combined Traditional Chinese and Western Medicine, Xiangya Hospital, Central South university, Changsha 410008, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Animals, Newborn;
Capillaries;
cytology;
Cell Hypoxia;
Cells, Cultured;
Cerebral Cortex;
blood supply;
Drugs, Chinese Herbal;
pharmacology;
Endothelium, Vascular;
cytology;
metabolism;
Female;
Male;
Rats;
Rats, Sprague-Dawley;
Serum;
Vascular Endothelial Growth Factor A;
biosynthesis;
genetics
- From:
Journal of Central South University(Medical Sciences)
2005;30(2):153-156
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To determine the effects of naoyian (NYA) serum on the expression of vascular endothelial growth factor (VEGF) protein in cultured rat cerebral microvascular endothelial cell (RCMEC) with hypoxia.
METHODS:NYA serum was separated from rat heart which had been filled stomach with NYA successively for 3 days. The rat cerebral microvascular endothelial cells were taken from the Sprageu-Dawley rat brain at postborn 7 days. The rat cerebral microvascular endothelial cells were incubated at anaerobic incubator to establish the hypoxia models. The vigo of RCMEC was determined by MTT. The level of expression of VEGF protein was measured by cell immunohistochemistry and Western blot.
RESULTS:The OD value of NYA serum group was higher than the control groups after hypoxia for 18 hours. VEGF protein was increased by hypoxia in cerebral microvascular endothelial cells (P < 0.05). The content of VEGF protein in NYA serum containing medium was more significantly elevated than those cultured in other control media (P < 0.01).
CONCLUSION:VEGF protein was induced by hypoxia in rat cerebral microvascular endothelial cells, and NYA could upregulate the expression of VEGF protein, which may be one of the protection mechanisms for cerebral microvascular endothelial cells.
