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Madecassoside, a triterpenoid saponin isolated from Centella asiatica herbs, protects endothelial cells against oxidative stress
Author(s) -
Bian Difei,
Liu Mei,
Li Ying,
Xia Yufeng,
Gong Zhunan,
Dai Yue
Publication year - 2012
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.21434
Subject(s) - oxidative stress , centella , apoptosis , malondialdehyde , viability assay , chemistry , mitochondrion , umbilical vein , p38 mitogen activated protein kinases , mapk/erk pathway , lactate dehydrogenase , pharmacology , biochemistry , microbiology and biotechnology , biology , kinase , in vitro , horticulture , enzyme
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. © 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:399–406, 2012; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.21434