Mesenchymal Stem Cells Decrease Oxidative Stress in the Bowels of Interleukin-10 Knockout Mice

氧化应激 超氧化物歧化酶 炎症 间充质干细胞 医学 活性氧 脂质过氧化 免疫学 病理 生物 内分泌学 细胞生物学
作者
Kyong Jin Jung,Gun Woo Lee,Chul Hyun Park,Tae Jin Lee,Joo‐Young Kim,Eon Gi Sung,Seong Yong Kim,Byung Ik Jang,In‐Hwan Song
出处
期刊:Gut and Liver [Korean Association for the Study of the Liver]
卷期号:14 (1): 100-107 被引量:27
标识
DOI:10.5009/gnl18438
摘要

Background/Aims: Inflammatory bowel disease (IBD) is an autoimmune disease characterized by chronic inflammation mainly in the large intestine. The interleukin-10 knockout (IL-10 KO) mouse is a well-known animal model of IBD that develops spontaneous intestinal inflammation resembling Crohn's disease. Oxidative stress is considered to be the leading cause of cell and tissue damage. Reactive oxygen species (ROS) can cause direct cell injury and/or indirect cell injury by inducing the secretion of cytokines from damaged cells. This study evaluated the effects of mesenchymal stem cell (MSC) on the progression of IBD. Methods: In this study, human bone marrow-derived MSCs were injected into IL-10 KO mice (MSC). Oxidative stress and inflammation levels were evaluated in the large intestine and compared with those in control IL-10 KO mice (CON) and normal wild-type control mice (Wild). Results: The levels of ROS (superoxide and hydrogen peroxidase) and a secondary end-product of lipid peroxidation (malondialdehyde) were considerably higher in the CON, while superoxide dismutase and catalase levels were lower in the MSC. Inflammation-related marker (interferon-γ, tumor necrosis factor-α, IL-4, and CD8) expression and inflammatory histological changes were much less pronounced in MSC than in CON. Conclusions: MSCs affect the redox balance, leading to the suppression of IBD.
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