Department of Pharmacy, Peking University Shenzhen Hospital, Shenzhen 518035, China.
School of Pharmaceutical Sciences, Health Science Center, Shenzhen University, Shenzhen 518060, China.
Oxid Med Cell Longev. 2018 Apr 10;2018:8549052. doi: 10.1155/2018/8549052. eCollection 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 -coumaric acid (-CA) on hydrogen peroxide- (HO-) induced apoptosis in human lens epithelial (HLE) cells (SRA 01-04). Cells were pretreated with -CA at a concentration of 3, 10, and 30 M before the treatment of HO (275 M). Results showed that pretreatment with -CA significantly protected against HO-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, -CA also greatly suppressed HO-induced intracellular ROS production and mitochondrial membrane potential loss and elevated the activities of T-SOD, CAT, and GSH-Px of HO-treated cells. As well, study showed that -CA also suppressed HO-induced phosphorylation of p-38, ERK, and JNK in HLE cells. These findings demonstrate that -CA suppresses HO-induced HLE cell apoptosis through modulating MAPK signaling pathways and suggest that -CA has a potential therapeutic role in the prevention of cataract.
防止氧化应激诱导的晶状体上皮细胞凋亡是预防白内障形成的一种潜在策略。本研究旨在研究对香豆酸（-CA）对人晶状体上皮（HLE）细胞（SRA 01-04）中过氧化氢（HO-）诱导的凋亡的保护作用及其潜在机制。细胞在 HO（275μM）处理前用 3、10 和 30μM 的 -CA 进行预处理。结果表明，-CA 预处理以剂量依赖性方式显著防止 HO 诱导的细胞死亡，并且下调 HLE 细胞中 cleaved caspase-3 和 cleaved caspase-9 的表达。此外，-CA 还极大地抑制了 HO 诱导的细胞内 ROS 产生和线粒体膜电位丧失，并提高了 HO 处理细胞的 T-SOD、CAT 和 GSH-Px 的活性。此外，研究表明 -CA 还抑制了 HO 诱导的 HLE 细胞中 p-38、ERK 和 JNK 的磷酸化。这些发现表明 -CA 通过调节 MAPK 信号通路抑制 HO 诱导的 HLE 细胞凋亡，并表明 -CA 在预防白内障方面具有潜在的治疗作用。
