L-Arginine Protects Ovine Intestinal Epithelial Cells from Lipopolysaccharide-Induced Apoptosis through Alleviating Oxidative Stress.

Abstract

This research aims to explore the effect of l-arginine (Arg) upon lipopolysaccharide (LPS)-induced induction of the oxidative stress as well as subsequent apoptosis within ovine intestinal epithelial cells (IOECs). Through a 16 h incubation, cells were divided into four groups and the medium was replaced with different medium as follows: (1) control (Con), Arg-free Dulbecco's modified Eagle's F12 Ham medium (DMEM); (2) Arg treatment, Arg-free DMEM supplemented with 100 μM Arg; (3) LPS treatment, Arg-free DMEM supplemented with 10 μg/mL LPS; (4) LPS with Arg treatment, Arg-free DMEM supplemented with both 10 μg/mL LPS and 100 μM Arg. After culturing for 24 h in different mediums, some characteristics of cells in the four groups were measured. Addition of Arg increased cell viability induced with LPS compared with the LPS group ( p < 0.05). Arg significantly decreased the release of dehydrogenase (LDH) and the production of malonaldehyde (MDA) ( p < 0.05) within IOECs challenged by the LPS. Compared with the LPS group, cells treated with Arg and Arg + LPS increased ( p < 0.05) mRNA as well as protein expression of glutathione peroxidase 1 (GPx1), catalase (CAT), superoxide dismutase 2 (SOD2), B-cell lymphoma 2 (Bcl2), quinone oxidoreductase 1 (NQO1), heme oxygenase (HO-1), and nuclear factor erythroid 2-related factor 2 (Nrf2). IOEC treatment with Arg reduced significantly ( p < 0.05) apoptosis induced by the LPS (12.58 ± 0.79%). The results showed that Arg promoted the protein expression of Nrf2, up-regulated expression of the phase II metabolizing enzymes (NQO1 and HO-1), as well as antioxidative enzymes (GPx1, CAT, and SOD2) for alleviating oxidative injury and protected IOECs from LPS-induced apoptosis.