trans-Polydatin protects the mouse heart against ischemia/reperfusion injury via inhibition of the renin-angiotensin system (RAS) and Rho kinase (ROCK) activity
trans-Polydatin protects the mouse heart against ischemia/reperfusion injury via inhibition of the renin-angiotensin system (RAS) and Rho kinase (ROCK) activity
复制标题
反式虎杖甙通过抑制肾素-血管紧张素系统 (RAS) 和 Rho 激酶 (ROCK) 活性，保护小鼠心脏免受缺血/再灌注损伤
DOI：
10.1039/c6fo01842d
复制
发表时间：
2017-06-01
期刊：
影响因子：
6.1
通讯作者：
Jie, Liu
中科院分区：
文献类型：
--
作者：
Ming, Dong;Songyan, Liao;Jie, Liu
背景资料：最近的研究强调了从虎杖中提取的中药提取物反式虎杖苷对心脏疾病的保护作用。本研究探讨了转肽酶对心肌缺血/再灌注（IR）损伤的治疗作用及其与肾素-血管紧张素系统（RAS）和RhoA激酶（ROCK）通路的关系。方法与结果：对新生大鼠心室肌细胞进行缺氧-复氧（模拟IR，SIR）实验，并对成年小鼠进行左冠状动脉前降支闭塞45分钟，然后再灌注一周的实验。反式白藜芦醇苷显著增加SIR心肌细胞的细胞活力并减少细胞凋亡。还观察到其减少IR小鼠的梗塞面积和增加心脏功能。反式白藜芦醇苷可降低血管紧张素的表达，抑制肾素和血管紧张素转换酶的活性。此外，反式虎杖苷抑制ROCK活性，特别是血管紧张素I受体激活的ROCK途径。结论：反式白藜芦醇苷可能通过抑制RAS和下游ROCK通路而发挥抗心肌IR损伤的心脏保护作用。
Background: Recent studies highlighted the protective benefits of a Chinese herb extract from polygonum cuspidatum, trans-polydatin, on cardiac disease. We investigated the therapeutic effect of transpolydatin on myocardial ischemia/reperfusion (IR) injury and the underlying mechanisms related to the renin-angiotensin system (RAS) and RhoA kinase (ROCK) pathway. Methods and results: Experiments were performed on neonatal rats' ventricular myocytes that were subjected to hypoxia-reoxygenation (simulated IR, SIR) and on adult mice which were subjected to left anterior descending coronary artery occlusion for 45 min followed by a one-week reperfusion. trans-Polydatin significantly increased cell viability and reduced apoptosis in SIR cardiomyocytes. It was also observed to reduce the infarct size and increase the cardiac function in IR mice. trans-Polydatin decreased the expression of angiotensin and inhibited the activities of renin and angiotensin-converting enzyme. Furthermore, trans-polydatin inhibited ROCK activity, especially the angiotensin I receptor-activated ROCK pathway. Conclusions: trans-Polydatin exerts a cardio-protection against myocardial IR injury likely through inhibiting both RAS and the downstream ROCK pathway.