Department of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, P.R. China.
Pharm Biol. 2012 Oct;50(10):1226-32. doi: 10.3109/13880209.2012.664555. Epub 2012 Aug 13.
Picroside II, an iridoid glucoside found in the root of Picrorhiza scrophulariiflora Pennell (Scrophulariaceae), has been demonstrated to possess potent antioxidant activity. However, whether picroside II has a protective effect against hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury is poorly understood.
To explore the cardioprotective role of picroside II against oxidative stress induced by H/R injury in neonatal rat cardiacmyocytes.
The viability and cellular damage of cardiomyocytes were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolim bromide (MTT) and lactate dehydrogenase (LDH) assays, respectively. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), the levels of reduced (GSH) and oxidized glutathione (GSSG), and the contents of malondialdehyde (MDA) were determined by a colorimetric method. The levels of intracellular reactive oxygen species (ROS) and calcium were evaluated by flow cytometric analysis.
We analyzed the effective half-maximal concentration for protection from the dose-response curves and obtained the concentration of 50 µg/mL as EC(50). Pretreated cardiomyocytes with picroside II (50-200 µg/mL), prior to H/R exposure, inhibited LDH activity in culture media and increased cell viability in a dose-dependent manner. This protective effect was accompanied by significantly increasing reduced GSH contents and the activities of SOD and GSH-Px and attenuating MDA and GSSG contents in response to H/R injury. Furthermore, treatment with picroside II also inhibited ROS production and calcium accumulation in cardiomyocytes.
The present study demonstrates that picroside II protects cardiomyocytes against oxidative-stress injury induced by H/R through reduction of ROS production and calcium accumulation and enhancement of the activity of antioxidant defense.
裂环环烯醚萜苷皮苦素 II 是玄参科獐牙菜属植物獐牙菜（Picrorhiza scrophulariiflora Pennell）中的环烯醚萜苷，具有很强的抗氧化活性。然而，皮苦素 II 对缺氧/复氧（H/R）诱导的心肌细胞损伤是否具有保护作用尚不清楚。
探讨皮苦素 II 对 H/R 损伤诱导的新生大鼠心肌细胞氧化应激的保护作用。
通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐（MTT）和乳酸脱氢酶（LDH）测定法分别评估心肌细胞活力和细胞损伤。超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）的活性、还原型（GSH）和氧化型谷胱甘肽（GSSG）的水平以及丙二醛（MDA）的含量通过比色法测定。通过流式细胞术分析评估细胞内活性氧（ROS）和钙的水平。
我们从剂量-反应曲线中分析了保护作用的有效半最大浓度，并获得了 50μg/mL 的浓度作为 EC（50）。在 H/R 暴露前，用皮苦素 II（50-200μg/mL）预处理心肌细胞，可抑制培养基中 LDH 的活性，并呈剂量依赖性增加细胞活力。这种保护作用伴随着还原型 GSH 含量的显著增加，以及 SOD 和 GSH-Px 的活性增强，并减轻了 H/R 损伤时 MDA 和 GSSG 的含量。此外，皮苦素 II 的治疗还抑制了心肌细胞中 ROS 的产生和钙的积累。
本研究表明，皮苦素 II 通过减少 ROS 产生和钙积累以及增强抗氧化防御的活性来保护心肌细胞免受 H/R 诱导的氧化应激损伤。
