Postconditioning’s protection of THSG on cardiac ischemia-reperfusion injury and mechanism

Abstract

2,3,5,4′-tetra-hydroxystilbene-2-O-glucoside (THSG), the water-soluble active components extracted from dried tuber root ofPolygonum multi florum (Polygonaceae), can promote the release of nitric oxide (NO) from vascular endothelial cells and has strong antioxidation. The post-conditioning'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 re-spectively. 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). SαT 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), SαT 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 K_ATP channel opening.

Keywords

THSG / postconditioning / ischemia-reperfusion injury / K_ATP

References

[1] ZhaoZ Q, CorveraJ S, HalkosM E, et al.. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol, 2004, 286(1): H477-H477

[2] YangX M, PhilippS, DowneyJ M, et al.. Postconditioning's protection is not dependent on circulating blood factors or cells but involves adenosine receptors and requires PI3-kinase and guanylyl cyclase activation. Basic Res Cardiol, 2005, 100(1): 57-63

[3] Vinten-JohansenJ, ZhaoZ Q, ZattaA J, et al.. Postconditioning: A new link in nature's armor against myocardial ischemia-reperfusion injury. Basic Res Cardiol, 2005, 100: 1-16

[4] LiuQ L, BanY, ZhangJ H, et al.. Influence of 2,3,5,4′-tetrahydroxystilbene-2-O-β-D-glucoside on vasodilation and nitric oxide content in rat aorta. Chin J Pharmacol Toxicol (Chinese), 2004, 18(4): 289-293

[5] YangX M, ProctorJ B, CuiL, et al.. Multiple, brief coronary occlusions during early reperfusion protect rabbit hearts by targeting cell signaling pathways. J Am Coll Cardiol, 2004, 44(5): 1103-1110

[6] GryerR M, HsuA K, GrossG J. Mitochondrial K (ATP) channel opening is important during index ischemia and following myocardial reperfusion in ischemic pre-conditioned rat hearts. J Mol Cell Cardiol, 2001, 33(4): 831-834

[7] BanY, LiuQ L, JinY, et al.. Determination of stilbene-glucoside and investigation on its stability. Zhong Cao Yao (Chinese), 2004, 18(4): 1235-1237

[8] TsangA, HausenloyD J, MocanuM M, et al.. Postconditioning: a form of “modified reperfusion” protects the myocardium by activating the phosphatidylinositol 3-kinase-Akt pathway. Circ Res, 2004, 95(3): 230-232

[9] GendaS, MiuraT, MikiT, et al.. K (ATP) channel opening is an endogenous mechanism of protection against the no-reflow phenomenon but its function is compromised by hypercholesterolemia. J Am Coll Cardiol, 2002, 40(7): 1339-1346