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

文献类型： 外文期刊

第一作者： Qiu, Yueqin

作者： Qiu, Yueqin;Yang, Xuefen;Wang, Li;Gao, Kaiguo;Jiang, Zongyong;Qiu, Yueqin;Yang, Xuefen;Wang, Li;Gao, Kaiguo;Jiang, Zongyong;Qiu, Yueqin;Yang, Xuefen;Wang, Li;Gao, Kaiguo;Jiang, Zongyong;Qiu, Yueqin;Yang, Xuefen;Wang, Li;Gao, Kaiguo;Jiang, Zongyong;Qiu, Yueqin;Yang, Xuefen;Wang, Li;Gao, Kaiguo;Jiang, Zongyong;Qiu, Yueqin

作者机构：

关键词： L-arginine; lipopolysaccharide; inflammatory effect; oxidative stress; Arginase-1

期刊名称：INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES （ 影响因子：5.923； 五年影响因子：6.132 ）

ISSN： 1422-0067

年卷期： 2019 年 20 卷 7 期

页码：

收录情况： SCI

摘要： 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-kappa Bp65), chemokine-8 (IL-8), tumor necrosis factor (TNF-alpha) 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-kappa Bp65, 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.

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