No abstract

We aim to investigate the effects of curcumin on preventing diabetes-induced vascular inflammation in association with its actions on Txnip, ICAM-1, and NOX2 enzyme expressions. Male Wistar rats were divided into four groups: control (CON), diabetic (DM; streptozotocin (STZ), i.v. 55 mg/kg BW), control-treated with curcumin (CONCUR; 300 mg/kg BW), and diabetes treated with curcumin (DMCUR; 300 mg/kg BW). 12th week after STZ injection, iris blood perfusion, leukocyte adhesion, Txnip, p47phox, and malondialdehyde (MDA) levels were determined by using laser Doppler, intravital fluorescent confocal microscopy, Western Blot analysis, and TBAR assay, respectively. The iris blood perfusion of DM and DMCUR was decreased significantly compared to CON and CONCUR (P < 0.001). Plasma glucose and HbA1c of DM and DMCUR were increased significantly compared to CON and CONCUR (P < 0.001). Leukocyte adhesion, ICAM-1, p47phox expression, and MDA levels in DM were increased significantly compared to CON, CONCUR, and DMCUR (P < 0.05). Txnip expression in DM and DMCUR was significantly higher than CON and CONCUR (P < 0.05). From Pearson's analysis, the correlation between the plasma MDA level and the endothelial functions was significant. It suggested that curcumin could ameliorate diabetic vascular inflammation by decreasing ROS overproduction, reducing leukocyte-endothelium interaction, and inhibiting ICAM-1 and NOX2 expression.

The correlation between endothelial function and reactive oxygen species detecting from diabetic microvascular wall and the antioxidant effect of ascorbic acid (AA) during early and late phases of diabetic induction were determined. Male Spraque-Dawley rats were divided into four groups: control, diabetes rats (DM, using iv.injection of 55 mg/kg BW streptozotocin, (STZ)), and two groups of DM rats treated with AA (1 g/L, (STZ)) starting on day 2 (DM + AAday2) and week 6th (DM + AA6wk). On 12th week after STZ injection, the findings showed that in DM group, Ach (10−5 M)-induced vasodilatation was decreased, while the number of leukocyte adhesion was increased significantly (P < 0.01). Interestingly, these abnormalities induced by DM could be protected or improved in both AA-treated groups, DM + AAday2 and DM + AA6wk. By using dihydrorhodamine 123, our findings also indicated that the existing of ROS productions on diabetic arteriolar and venular walls were different significantly (ROSarteriole = 165.89 ± 24.59 and ROSvenule = 172.26 ± 34.70) (P < 0.05). Moreover by using BH4 inhibitor to induce increase in arteriolar ROS, the results also confirmed that AA could improve endothelial function with closed correlation to its potential to reduce vascular ROS content.