L‑carnitine alleviates oxidative stress‑related damage via MAPK signaling in human lens epithelial cells exposed to H2O2.

Abstract

L‑carnitine (LC) is well known for its antioxidative properties. The present study aimed to evaluate the effects of LC on human lens epithelial cells (HLECs) and to analyze its regulatory mechanism in cataractogenesis. HLE B‑3 cells were cultured with hydrogen peroxide (H2O2) and were pretreated with or without LC. The Cell Counting kit‑8 assay was used to determine cell viability. Reactive oxygen species(ROS) assay kit was used to measure the cellular ROS production induced by H2O2 and LC. In addition, reverse transcription‑quantitative PCR and western blot analysis were performed to detect the expression levels of oxidative damage markers and antioxidant enzymes. Notably, ROS overproduction was observed upon exposure to H2O2, whereas LC supplementation markedly decreased ROS levels through activation of the antioxidant enzymes forkhead box O1, peroxiredoxin 4 and catalase. Furthermore, LC suppressed the expression of apoptosis‑associated genes (caspase-3) and inflammation‑associated genes [interleukin(IL)1, IL6, IL8 and cyclooxygenase‑2]. Conversely, LC promoted proliferating cell nuclear antigen, cyclin‑dependent kinase (CDK)2 and CDK4 expression, which may increase proliferation of HLECs that were incubated with H2O2. In addition, epithelial‑mesenchymal transition occurred upon ROS accumulation, whereas the effects of H2O2 on AQP1 and vimentin expression were reversed upon LC supplementation. Notably, this study revealed that LC restored the oxidant/antioxidant balance and protected against cell damage through the mitogen‑activated protein kinase signaling pathway. In conclusion, LC may serve a protective role in curbing oxidative damage and therefore may be considered a potential therapeutic agent for the treatment of cataracts.