We investigated the effect of cyanidin-3-rutinoside (C3R) against methylglyoxal (MG)-advanced glycation end products (AGEs) mediated cardio-vascular abnormalities in rats pre-treated with MG. In the rats, plasma MG level rose following oral administration of MG (60–120 mg/rat/day) for 8 weeks and was accompanied by a buildup of MG-derived AGE, N^ɛ-(carboxymethyl) lysine, in aortic tissue both of which were decreased by co-treatment with C3R (30 and 100 mg/kg/day). Similarly, MG-impaired vascular contraction/relaxation responses were normalized by C3R with concomitant upregulation of endothelial nitric oxide synthase mRNA expression. In the whole animal subjected to coronary artery ligation, C3R (100 mg/kg/day) reduced ventricular extra beats and ventricular tachycardia precipitated during acute ischemic episode. We suggest that C3R reduces the formation and accumulation of AGEs via direct trapping of the MG and upregulation of mRNA expression of glyoxalase I. The findings implicate C3R as a candidate compound for preventing MG-AGE mediated cardiovascular abnormalities in diabetes.

我们调查了花青素-3-芸苔苷（C3R）对甲基乙二醛（MG）-先进的糖基化终产物（AGEs）介导的用MG预处理的大鼠的心血管异常的影响。在大鼠中，口服MG（60-120 mg /大鼠/天）8周后血浆MG水平升高，并伴有MG衍生的AGE，N ^build-（羧甲基）赖氨酸，在主动脉组织中都通过与C3R（30和100 mg / kg / day）共同处理而降低。同样，MG受损的血管收缩/松弛反应可通过C3R正常化，同时伴随内皮一氧化氮合酶mRNA表达的上调。在接受冠状动脉结扎的整个动物中，C3R（100 mg / kg /天）减少了急性缺血发作期间的心室多余搏动和心室心动过速。我们建议C3R通过直接捕获MG和乙二醛酶I的mRNA表达上调来减少AGEs的形成和积累。该发现暗示C3R作为预防MG-AGE介导的糖尿病性心血管疾病的候选化合物。