State Key Laboratory of Natural Medicines, Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing 210009, People's Republic of China.
J Biochem Mol Toxicol. 2012 Oct;26(10):399-406. doi: 10.1002/jbt.21434. Epub 2012 Jul 24.
This study aimed to investigate the effect of madecassoside against oxidative stress-induced injury of endothelial cells. Hydrogen peroxide (H(2)O(2), 500 µmol/L) was employed as an inducer of oxidative stress in human umbilical vein endothelial cells (HUVECs). Cell apoptosis was detected by Hoechst 33258 staining and flow cytometry. Caspase-3 activity and mitochondria membrane potential were further examined. As a result, madecassoside (10, 30, 100 µmol/L) could reverse morphological changes, elevate cell viability, increase glutathione levels, and decrease lactate dehydrogenase and malondialdehyde levels caused by H(2)O(2) in a concentration-dependent manner. It attenuated apoptosis, preventing the activation of caspase-3 and the loss of mitochondria membrane potential, as well as the phosphorylation of p38 mitogen-activated protein kinase (MAPK) in HUVECs. These data suggested that madecassoside could protect HUVECs from oxidative injury, which was probably achieved by inhibiting cell apoptosis via protection of mitochondria membranes and downregulation of the activation of caspase-3 and p38 MAPK.
本研究旨在探讨积雪草苷对氧化应激诱导的内皮细胞损伤的作用。过氧化氢（H₂O₂，500μmol/L）被用作人脐静脉内皮细胞（HUVECs）氧化应激的诱导剂。采用 Hoechst 33258 染色和流式细胞术检测细胞凋亡。进一步检测 caspase-3 活性和线粒体膜电位。结果表明，积雪草苷（10、30、100μmol/L）可逆转 H₂O₂引起的形态变化，提高细胞活力，增加谷胱甘肽水平，降低乳酸脱氢酶和丙二醛水平，呈浓度依赖性。它抑制细胞凋亡，防止 caspase-3 的激活和线粒体膜电位的丧失，以及 p38 丝裂原活化蛋白激酶（MAPK）的磷酸化，从而减轻 HUVECs 的凋亡。这些数据表明，积雪草苷可以保护 HUVECs 免受氧化损伤，这可能是通过保护线粒体膜和下调 caspase-3 和 p38 MAPK 的激活来实现的。
