Ginsenoside Rb 1 Reduces Hyper-Vasoconstriction Induced by High Glucose and Endothelial Dysfunction in Rat Aorta.

Acute hyperglycemia induces oxidative damage and inflammation, leading to vascular dysfunction. Ginsenoside Rb 1 (Rb 1 ) is a major component of red ginseng with anti-diabetic, anti-oxidant and anti-inflammatory properties. Here, we investigated the beneficial effects and the underlying mechanisms of Rb 1 on hypercontraction induced by high glucose (HG) and endothelial dysfunction (ED). The isometric tension of aortic rings was measured by myography. The rings were treated with N G -nitro-L-arginine methyl ester (L-NAME) to induce chemical destruction of the endothelium, and Rb 1 was added after HG induction. The agonist-induced vasoconstriction was significantly higher in the aortic rings treated with L-NAME + HG50 than in those treated with HG50 or L-NAME ( p = 0.011) alone. Rb 1 significantly reduced the hypercontraction in the aortic rings treated with L-NAME + HG50 ( p = 0.004). The ATP-sensitive K + channel (K ATP ) blocker glibenclamide tended to increase the Rb 1 -associated reduction in the agonist-induced vasoconstriction in the rings treated with L-NAME + HG50. The effect of Rb 1 in the aortic rings treated with L-NAME + HG50 resulted from a decrease in extracellular Ca 2+ influx through the receptor-operated Ca 2+ channel (ROCC, 10 -6 -10 -4 M CaCl 2 , p < 0.001; 10 -3 -2.5 × 10 -3 M CaCl 2 , p = 0.001) and the voltage-gated Ca 2+ channel (VGCC, 10 -6 M CaCl 2 , p = 0.003; 10 -5 -10 -2 M CaCl 2 , p < 0.001), whereas Rb 1 did not interfere with Ca 2+ release from the sarcoplasmic reticulum. In conclusion, we found that Rb 1 reduced hyper-vasoconstriction induced by HG and ED by inhibiting the ROCC and the VGCC, and possibly by activating the K ATP in rat aorta. This study provides further evidence that Rb 1 could be developed as a therapeutic target for ED in diabetes.