p-Coumaric Acid Protects Human Lens Epithelial Cells against Oxidative Stress-Induced Apoptosis by MAPK Signaling.
Jiao PengTing-Ting ZhengYue LiangLi-Fang DuanYao-Dong ZhangLi-Jun WangGuang-Ming HeHai-Tao XiaoPublished in: Oxidative medicine and cellular longevity (2018)
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 μM before the treatment of H2O2 (275 μM). 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.
Keyphrases
- induced apoptosis
- signaling pathway
- oxidative stress
- endoplasmic reticulum stress
- diabetic rats
- pi k akt
- cell death
- epithelial mesenchymal transition
- endothelial cells
- dna damage
- high glucose
- hydrogen peroxide
- protein kinase
- cell proliferation
- nitric oxide
- induced pluripotent stem cells
- newly diagnosed
- fluorescent probe