Cytoprotective effects of diosmetin against hydrogen peroxide-induced L02 cell oxidative damage via activation of the Nrf2-ARE signaling pathway

作者：Chunjing Wang, Yaping Liao, Shengnan Wang, Dan Wang, Nana Wu, Qingao Xu, Wanwan Jiang, Menran Qiu, Changqing Liu · 发表于：Molecular Medicine Reports · 年份：2018 · DOI：10.3892/mmr.2018.8750 · 被引用次数：29 · 研究领域：Genomics, phytochemicals, and oxidative stress、Drug-Induced Hepatotoxicity and Protection、Vitamin C and Antioxidants Research

Oxidative stress is considered a crucial mediator in the pathogenesis of various liver diseases. The flavone diosmetin has been reported to exhibit antioxidant activities; however, the hepatoprotective effects of diosmetin against oxidative stress, and the underlying molecular mechanisms, remain unknown. The present study aimed to investigate the potential hepatoprotective effects of diosmetin on hydrogen peroxide (H2O2)‑induced oxidative damage in L02 cells and attempted to evaluate the role of the nuclear factor erythroid 2‑related factor 2 (Nrf2)/antioxidant response element pathway in this process. L02 cells were divided into groups: Control (DMSO, diosmetin), H2O2, Trolox or tertiary butylhydroquinone and diosmetin (different doses). Protective effects in L02 cells were determined by CCK‑8, cell apoptosis and lactate dehydrogenase leakage assays. Flow cytometry and inverted fluorescence microscope were used to measure the intracellular reactive oxygen species (ROS) and mitochondrial membrane potential (MMP). Protein expression levels were of Nrf2, heme oxygenase‑1 (HO‑1) and NAD(P)H quinone oxidoreductase‑1 (NQO1) were determined by western blotting and mRNA levels were determined by reverse transcription‑quantitative polymerase chain reaction. The results revealed that H2O2 induced notable injury to L02 cells, as demonstrated by decreased cell viability, increased lactate dehydrogenase release, apoptotic rate and intracellular ROS production, and by the loss of MMP. Con...