Journal
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
Volume 2018, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2018/8549052
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Funding
- National Natural Science Foundation of China [81660479, 21102025]
- Natural Research Platform of the Department of Education, Guizhou Province, China [2016-004]
- launching fund of Scientific Research for New Teachers of Shenzhen University [2018020]
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To protect against oxidative stress-induced apoptosis in lens epithelial cells is a potential strategy in preventing cataract formation. The present study aimed at studying the protective effect and underlying mechanisms of p-coumaric acid (p-CA) on hydrogen peroxide-(H2O2-) induced apoptosis in human lens epithelial (HLE) cells (SRA 01-04). Cells were pretreated with p-CA at a concentration of 3, 10, and 30 mu M before the treatment of H2O2 (275 mu M). Results showed that pretreatment with p-CA significantly protected against H2O2-induced cell death in a dose-dependent manner, as well as downregulating the expressions of both cleaved caspase-3 and cleaved caspase-9 in HLE cells. Moreover, p-CA also greatly suppressed H2O2-induced intracellular ROS production and mitochondrial membrane potential loss and elevated the activities of T-SOD, CAT, and GSH-Px of H2O2-treated cells. As well, in vitro study showed that p-CA also suppressed H2O2-induced phosphorylation of p-38, ERK, and JNK in HLE cells. These findings demonstrate that p-CA suppresses H2O2-induced HLE cell apoptosis through modulating MAPK signaling pathways and suggest that p-CA has a potential therapeutic role in the prevention of cataract.
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