2,3,5,4＇-tetra-hydroxystilbene-2-O-glucoside （THSG）, the water-soluble active components extracted from dried tuber root of Polygonum multiflorurn （Polygonaceae）, can promote the release of nitric oxide （NO） fr...2,3,5,4＇-tetra-hydroxystilbene-2-O-glucoside （THSG）, the water-soluble active components extracted from dried tuber root of Polygonum multiflorurn （Polygonaceae）, can promote the release of nitric oxide （NO） from vascular endothelial cells and has strong antioxidation. The postconditioning＇s protection of THSG on cardiac ischemia-reperfusion injury and the mechanism were investigated. After reperfusion for 3 h following occlusion of rat left anterior descending coronary artery （LAD） for 30 min, SαT recovery speed, arrhythmia and cardiac infarct size were observed. The ischemic size and infarct size was identified by using Evans blue and TTC staining methods respectively. The results showed that the infarct size in THSG 7.5 mg/kg postconditioning group was significantly decreased from 43.6 %± 9.1% in mode group to 16.5% ±6.5% （P〈0.01）. SaT recovery was quicker and the incidence of arrhythmia （55.6 % vs 100 %, P〈0.05） was significantly lower than in control group. The infarct size in THSG＋glybenclamide group was greater than in THSG group, but equivalent to that in control group （46.8 %±9.8 % vs 43. 6 %±9.1%, P〉0. 05）, SaT recovery speed slower and the incidence of arrhythmia also lower （33.3% vs 100%, P〈0.01）, suggesting that glybenclamide could abolish the effects of THSG postconditioning reducing the cardiac infart size. It was concluded that THSG administration before reperfusion could effectively alleviate the cardiac reperfusion injury and possessed the postconditioning effects of reducing cardiac infarct size, which might be related with the KATe channel opening.展开更多
文摘2,3,5,4＇-tetra-hydroxystilbene-2-O-glucoside （THSG）, the water-soluble active components extracted from dried tuber root of Polygonum multiflorurn （Polygonaceae）, can promote the release of nitric oxide （NO） from vascular endothelial cells and has strong antioxidation. The postconditioning＇s protection of THSG on cardiac ischemia-reperfusion injury and the mechanism were investigated. After reperfusion for 3 h following occlusion of rat left anterior descending coronary artery （LAD） for 30 min, SαT recovery speed, arrhythmia and cardiac infarct size were observed. The ischemic size and infarct size was identified by using Evans blue and TTC staining methods respectively. The results showed that the infarct size in THSG 7.5 mg/kg postconditioning group was significantly decreased from 43.6 %± 9.1% in mode group to 16.5% ±6.5% （P〈0.01）. SaT recovery was quicker and the incidence of arrhythmia （55.6 % vs 100 %, P〈0.05） was significantly lower than in control group. The infarct size in THSG＋glybenclamide group was greater than in THSG group, but equivalent to that in control group （46.8 %±9.8 % vs 43. 6 %±9.1%, P〉0. 05）, SaT recovery speed slower and the incidence of arrhythmia also lower （33.3% vs 100%, P〈0.01）, suggesting that glybenclamide could abolish the effects of THSG postconditioning reducing the cardiac infart size. It was concluded that THSG administration before reperfusion could effectively alleviate the cardiac reperfusion injury and possessed the postconditioning effects of reducing cardiac infarct size, which might be related with the KATe channel opening.
