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牛磺熊去氧胆酸对 RAW 264.7 巨噬细胞、骨髓来源的巨噬细胞、BV2 小胶质细胞和脊髓损伤的抗炎作用。

Anti-inflammatory effect of Tauroursodeoxycholic acid in RAW 264.7 macrophages, Bone marrow-derived macrophages, BV2 microglial cells, and spinal cord injury.

机构信息

Department of Neurosurgery, CHA University, CHA Bundang Medical Center, Seongnam-si, Gyeonggi-do, Republic of Korea.

Department of Biomedical Science, CHA University, Seongnam-si, Gyeonggi-do, Republic of Korea.

出版信息

Sci Rep. 2018 Feb 16;8(1):3176. doi: 10.1038/s41598-018-21621-5.

DOI:10.1038/s41598-018-21621-5
PMID:29453346
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5816629/
Abstract

This study aimed to investigate the anti-inflammatory effects of tauroursodeoxycholic acid (TUDCA) after spinal cord injury (SCI) in rats. We induced an inflammatory process in RAW 264.7 macrophages, BV2 microglial cells, and bone marrow-derived macrophages (BMM) using lipopolysaccharide (LPS). The anti-inflammatory effects of TUDCA on LPS-stimulated RAW 264.7 macrophages, BV2 microglial cells, and BMMs were analyzed using nitric oxide (NO) assays, quantitative real-time polymerase chain reactions (qRT-PCR), and enzyme-linked immunosorbent assays (ELISA). The pathological changes in lesions of the spinal cord tissue were evaluated by hematoxylin & eosin (H&E) staining, luxol fast blue/cresyl violet-staining and immunofluorescent staining. TUDCA decreased the LPS-stimulated inflammatory mediator, NO. It also suppressed pro-inflammatory cytokines of tumor necrosis factor-α (TNF-α), interleukin 1-β (IL-1β), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) in both mRNA and protein levels. In addition, TUDCA decreased prostaglandin E (PGE). After SCI, TUDCA supported the recovery of the injury site and suppressed the expression of inflammatory cytokines such as iNOS, CD68 and CD86. In addition, TUDCA induced the expression of anti-inflammatory cytokine, Arg-1. In conclusion, TUDCA inhibits inflammatory responses in RAW 264.7 macrophages, BV2 microglial cells, and BMMs. TUDCA can be a potential alternative drug for SCI.

摘要

本研究旨在探讨牛磺熊去氧胆酸（TUDCA）在大鼠脊髓损伤（SCI）后的抗炎作用。我们使用脂多糖（LPS）诱导 RAW 264.7 巨噬细胞、BV2 小胶质细胞和骨髓来源的巨噬细胞（BMM）中的炎症过程。使用一氧化氮（NO）测定、定量实时聚合酶链反应（qRT-PCR）和酶联免疫吸附测定（ELISA）分析 TUDCA 对 LPS 刺激的 RAW 264.7 巨噬细胞、BV2 小胶质细胞和 BMM 的抗炎作用。通过苏木精和伊红（H&E）染色、卢索快速蓝/固紫染色和免疫荧光染色评估脊髓组织损伤病变的病理变化。TUDCA 降低了 LPS 刺激的炎症介质 NO。它还抑制了肿瘤坏死因子-α（TNF-α）、白细胞介素 1-β（IL-1β）、环氧化酶-2（COX-2）和诱导型一氧化氮合酶（iNOS）的促炎细胞因子在 mRNA 和蛋白水平上的表达。此外，TUDCA 降低了前列腺素 E（PGE）的水平。在 SCI 后，TUDCA 支持损伤部位的恢复，并抑制了 iNOS、CD68 和 CD86 等炎症细胞因子的表达。此外，TUDCA 诱导了抗炎细胞因子 Arg-1 的表达。总之，TUDCA 抑制 RAW 264.7 巨噬细胞、BV2 小胶质细胞和 BMM 中的炎症反应。TUDCA 可能是 SCI 的一种潜在替代药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/495e/5816629/af13a323dfeb/41598_2018_21621_Fig8_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/495e/5816629/bef78d1809e4/41598_2018_21621_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/495e/5816629/eb2cd6f13342/41598_2018_21621_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/495e/5816629/225db87f2c1a/41598_2018_21621_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/495e/5816629/63175d4e4a1b/41598_2018_21621_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/495e/5816629/af13a323dfeb/41598_2018_21621_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/495e/5816629/44a656f09f9d/41598_2018_21621_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/495e/5816629/bef78d1809e4/41598_2018_21621_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/495e/5816629/69d44109d3d6/41598_2018_21621_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/495e/5816629/2290b6a25248/41598_2018_21621_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/495e/5816629/eb2cd6f13342/41598_2018_21621_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/495e/5816629/225db87f2c1a/41598_2018_21621_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/495e/5816629/63175d4e4a1b/41598_2018_21621_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/495e/5816629/af13a323dfeb/41598_2018_21621_Fig8_HTML.jpg

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