L-Arginine Inhibited Inflammatory Response and Oxidative Stress Induced by Lipopolysaccharide via Arginase-1 Signaling in IPEC-J2 Cells

Abstract

This study aimed to explore the effect of L-arginine on lipopolysaccharide (LPS)-induced inflammatory response and oxidative stress in IPEC-2 cells. We found that the expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), cluster of differentiation 14 (CD14), nuclear factor-kappaBp65 (NF-κBp65), chemokine-8 (IL-8), tumor necrosis factor (TNF-α) and chemokine-6 (IL-6) mRNA were significantly increased by LPS. Exposure to LPS induced oxidative stress as reactive oxygen species (ROS) and malonaldehyde (MDA) production were increased while glutathione peroxidase (GSH-Px) were decreased in LPS-treated cells compared to those in the control. LPS administration also effectively induced cell growth inhibition through induction of G0/G1 cell cycle arrest. However, compared with the LPS group, cells co-treatment with L-arginine effectively increased cell viability and promoted the cell cycle into the S phase; L-arginine exhibited an anti-inflammatory effect in alleviating inflammation induced by LPS by reducing the abundance of TLR4, MyD88, CD14, NF-κBp65, and IL-8 transcripts. Cells treated with LPS+L-arginine significantly enhanced the content of GSH-Px, while they decreased the production of ROS and MDA compared with the LPS group. Furthermore, L-arginine increased the activity of arginase-1 (Arg-1), while Arg-1 inhibitor abolished the protection of arginine against LPS-induced inflammation and oxidative stress. Taken together, these results suggested that L-arginine exerted its anti-inflammatory and antioxidant effects to protect IPEC-J2 cells from inflammatory response and oxidative stress challenged by LPS at least partly via the Arg-1 signaling pathway.

Human Postprandial Nutrient Metabolism and Low-Grade Inflammation: A Narrative Review

“…For example, the amino acid glutamine inhibits Nf-κB [52] and also lowers LPS-stimulated TNF-α production in intestinal epithelial cells (rat) [53] and glycine inhibits oxidative stress in porcine intestinal cells [54]. Arginine inhibited the LPS-induced inflammatory response and oxidative stress in vitro [55]. In contrast, the dietary supplementation of arginine resulted in an altered intestinal microbiota which, in turn, resulted in the activation of intestinal immunity, including the upregulation of TLR4 and Nf-kB protein expression in mice [56].…”

N-Carbamylglutamate and l-arginine supplementation improve hepatic antioxidant status in intrauterine growth-retarded suckling lambs

“…14 Thus, Arg may help relieve the health-and developmental-related issues that IUGR causes. 15,16 For instance, Arg can regulate synthesis of proteins and control the transduction of signals; 17 enhance production performance in livestock breeding; 18 suppress inammatory cytokines such as IL-6 and TNF-a; 19 and attenuate hepatic and plasma OS responses. 20 N-Carbamylglutamate (NCG), the analogue of N-acetylglutamate synthase (NAG), is metabolically stable and can help increase both plasma Arg concentrations and endogenous synthesis via activating the carbamoylphosphate synthase-1 and pyrroline-5 carboxylate synthase.…”

A possible role for inducible arginase isoform (AI) in the pathogenesis of chronic venous leg ulcer

“…Arginine has antimicrobial and anti-inflammatory properties (Meng, Cooney, Yepuri, & Cooney, 2017). Recently, (Qiu, Yang, Wang, Gao, & Jiang, 2019) have reported that the anti-inflammatory and antioxidant role of arginine occur via AI signaling pathway.…”