Protective Effect Of Aminoguanidine On Vascular Endothelial Function Of Glycosylated Proteins And Its Mechanisms,

AIM This study was designed to investigate the effect of aminoguanidine, an inhibitor of the glycosylated proteins formation, on the impairment of endothelium-dependent relaxation induced by advanced glycosylated end products (AGE) in isolated rat thoracic aorta and its possible mechanisms. METHODS Exogenous glycosylated bovine serum albumin (GBSA) was prepared. Exposure aortic rings to exogenous glycosylated bovine serum albumin (GBSA) for 60 min to induced the impairment of endothelium-dependent vasodilatation. In the drug-treating groups, aortic rings were incubated with drug for 15 min vand then exposed to GBSA for another 60 min in the presence of drug. Vasodilator responses to acetylcholine (ACh) or sodium nitroprusside (SNP) of aortic rings were measured by isometric tension recordings after drug treatment. RESULTS GBSA significantly inhibited the endothelium-dependent relaxation in response to ACh, but did not affect endothelium-independent relaxation in response to SNP. Pre-incubation of aortic rings with aminoguanidine (50 ~ 500 umol ?L-1) for 15 min and co-incubation of aortic rings with GBSA for another 60 min markedly attenuated the inhibition of relaxation induced by GBSA in a dose-dependent manner. Moreover, Superoxide diamutase (SOD 200 U ?mL-1), a scavenger of superoxide anions, also prevented the inhibition of relaxation, which is similar to the protection of 500 umol ?L-1 aminoguanidine. Furthermore, aminoguanidine (500 umol ?L-1) also reversed the impairment of endothelium-dependent relaxation of rat aortic rings induced by generated endogenous oxygen free radicals stimulated by diethyldithiocarbamate (DETC 10 umol ?L-1), an inhibitor of SOD. CONCLUSIONS Aminoguanidine can protect rat aortic endothelium against damage due to GBSA in vitro, and the beneficial effect of aminoguanidine may relate to its antioxidant properties.