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白细胞介素-13 通过氧化应激在体内介导凝血酶原 Kringle-2 诱导的海马神经毒性。

Interleukin-13 Propagates Prothrombin Kringle-2-Induced Neurotoxicity in Hippocampi In Vivo via Oxidative Stress.

机构信息

Department of Biochemistry and Molecular Biology, School of Medicine, Kyung Hee University, Seoul 02447, Korea.

Department of Neuroscience, Graduate School, Kyung Hee University, Seoul 02447, Korea.

出版信息

Int J Mol Sci. 2021 Mar 27;22(7):3486. doi: 10.3390/ijms22073486.

DOI:10.3390/ijms22073486
PMID:33801783
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8036367/
Abstract

The present study investigated expression of endogenous interleukin-13 (IL-13) and its possible function in the hippocampus of prothrombin kringle-2 (pKr-2)-lesioned rats. Here we report that intrahippocampal injection of pKr-2 revealed a significant loss of NeuN-immunopositive (NeuN) and Nissl cells in the hippocampus at 7 days after pKr-2. In parallel, pKr-2 increased IL-13 levels, which reached a peak at 3 days post pKr-2 and sustained up to 7 days post pKr-2. IL-13 immunoreactivity was seen exclusively in activated microglia/macrophages and neutrophils, but not in neurons or astrocytes. In experiments designed to explore the involvement of IL-13 in neurodegeneration, IL-13 neutralizing antibody (IL-13Nab) significantly increased survival of NeuN and Nissl cells. Accompanying neuroprotection, immunohistochemical analysis indicated that IL-13Nab inhibited pKr-2-induced expression of inducible nitric oxide synthase and myeloperoxidase within activated microglia/macrophages and neutrophils, possibly resulting in attenuation of reactive oxygen species (ROS) generation and oxidative damage of DNA and protein. The current findings suggest that the endogenous IL-13 expressed in pKr-2 activated microglia/macrophages and neutrophils might be harmful to hippocampal neurons via oxidative stress.

摘要

本研究探讨了内源性白细胞介素-13 (IL-13) 在凝血酶原酶 Kringle-2 (pKr-2) 损伤大鼠海马中的表达及其可能的功能。我们报告称，pKr-2 海马内注射显示在 pKr-2 后 7 天海马内 NeuN 免疫阳性 (NeuN) 和尼氏细胞明显丢失。同时，pKr-2 增加了 IL-13 水平，在 pKr-2 后 3 天达到峰值，并持续到 pKr-2 后 7 天。IL-13 免疫反应仅见于活化的小胶质细胞/巨噬细胞和中性粒细胞，而不是神经元或星形胶质细胞。在设计用于探索 IL-13 在神经退行性变中的作用的实验中，IL-13 中和抗体 (IL-13Nab) 显著增加了 NeuN 和尼氏细胞的存活。伴随神经保护作用，免疫组织化学分析表明，IL-13Nab 抑制了 pKr-2 诱导的活化小胶质细胞/巨噬细胞和中性粒细胞中诱导型一氧化氮合酶和髓过氧化物酶的表达，可能导致活性氧 (ROS) 生成和 DNA 和蛋白质氧化损伤减弱。目前的研究结果表明，pKr-2 激活的小胶质细胞/巨噬细胞和中性粒细胞中表达的内源性 IL-13 可能通过氧化应激对海马神经元造成损害。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b4a/8036367/ce6ec60662be/ijms-22-03486-g005.jpg
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