Protection of puerarin on impaired vascular endothelial function induced by glycosylated protein
- Author:
Hua-Fei DENG
1
Author Information
- Publication Type:Journal Article
- Keywords: Endothelial function; Endothelium-dependent relaxation; Glycosylated bovine serum albumin; Puerarin; Rabbit; Thoracic aorta
- From: Chinese Pharmaceutical Journal 2014;49(7):559-563
- CountryChina
- Language:Chinese
- Abstract: OBJECTIVE: To investigate the effects of puerarin on impaired endothelium-dependent relaxation induced by glycosylated bovine serum albumin (GBSA) in rabbit thoracic aorta and its mechanisms. METHODS: The rings were incubated with GBSA for 30 min to induce endothelial dysfunction, and with puerarin(0.25, 0.5 and 1 g · L-1), A-nitro-L-arginine methyl ester (L-NAME, 30 νmol · L-1), and indomethacin(10 μmol · L-1) to investigate the protective effect of puerarin on impaired vascular endothelial function elicited by GBSA, and the effect of L-NAME and indomethacin on the protective effect of puerarin. Moreover, the content of nitric oxide (NO) and malonaldehyde (MDA) and the activity of superoxide dismutase(SOD) in the rings were measured. RESULTS: Exposure of aortic rings to GBSA (200 mg · L-1) for 30 min resulted in a significant inhibition of endothelium-dependent relaxation, but had no affect on endothelium-independent relaxation. GBSA significantly decreased the level of NO and the activity of SOD but hugely increased the content of MDA in vascular tissues. Pre-incubation of aortic rings with puerarin markedly attenuated the inhibition of endothelium-dependent relaxation induced by GBSA. This protective effect of puerarin (1 g · L-1) was partially inhibited by L-NAME but not by indomethacin. Puerarin obviously increased NO level and SOD activity but evidently decreased MDA content in rings. CONCLUSION: Puerarin can protect against vascular endothelial dysfunction caused by GBSA and its mechanisms may be related to enhancing NO synthesis and its anti-oxidation.
