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Exposure to hyperbaric oxygen induces tumour necrosis factor-alpha (TNF-alpha) secretion from rat macrophages.暴露于高压氧会诱导大鼠巨噬细胞分泌肿瘤坏死因子-α(TNF-α)。
Clin Exp Immunol. 1995 Dec;102(3):655-9. doi: 10.1111/j.1365-2249.1995.tb03867.x.
2
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Hyperbaric oxygen activates discoidin domain receptor 2 via tumour necrosis factor-alpha and the p38 MAPK pathway to increase vascular smooth muscle cell migration through matrix metalloproteinase 2.高压氧通过肿瘤坏死因子-α和p38丝裂原活化蛋白激酶途径激活盘状结构域受体2,以通过基质金属蛋白酶2增加血管平滑肌细胞迁移。
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Differential effects of LPS, IFN-gamma and TNF alpha on the secretion of lysozyme by individual human mononuclear phagocytes: relationship to cell maturity.脂多糖、γ干扰素和肿瘤坏死因子α对单个人类单核吞噬细胞溶菌酶分泌的不同影响:与细胞成熟度的关系。
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本文引用的文献

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Effect of a single exposure to hyperbaric oxygen on blood mononuclear cells in human subjects.单次暴露于高压氧对人体血液单核细胞的影响。
Undersea Hyperb Med. 1993 Sep;20(3):197-204.
2
Effect of hyperbaric oxygen on tissue distribution of mononuclear cell subsets in the rat.高压氧对大鼠单核细胞亚群组织分布的影响。
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Increased oxygen tensions influence subset composition of the cellular immune system in aged mice.氧张力增加会影响老年小鼠细胞免疫系统的亚群组成。
Cancer Biother. 1994 Spring;9(1):39-54. doi: 10.1089/cbr.1994.9.39.
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Increased oxygen tensions modulate the cellular composition of the adaptive immune system in BALB/c mice.增加的氧张力调节BALB/c小鼠适应性免疫系统的细胞组成。
Cancer Biother. 1993 Fall;8(3):241-52. doi: 10.1089/cbr.1993.8.241.
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Endotoxin pretreatment of human monocytes alters subsequent endotoxin-triggered release of inflammatory mediators.人单核细胞的内毒素预处理会改变随后内毒素触发的炎症介质释放。
Shock. 1995 Apr;3(4):252-8. doi: 10.1097/00024382-199504000-00002.
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Immunosuppression by hyperbaric oxygen.高压氧引起的免疫抑制。
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Potection from oxygen toxicity with endotoxin. Role of the endogenous antioxidant enzymes of the lung.内毒素对氧中毒的防护作用。肺内源性抗氧化酶的作用。
J Clin Invest. 1980 May;65(5):1104-10. doi: 10.1172/JCI109763.
8
Human lymphotoxin.人淋巴毒素
Methods Enzymol. 1985;116:441-8. doi: 10.1016/s0076-6879(85)16035-0.
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Secretory products of macrophages.巨噬细胞的分泌产物。
J Clin Invest. 1987 Feb;79(2):319-26. doi: 10.1172/JCI112815.
10
Recombinant tumor necrosis factor/cachectin and interleukin 1 pretreatment decreases lung oxidized glutathione accumulation, lung injury, and mortality in rats exposed to hyperoxia.重组肿瘤坏死因子/恶病质素和白细胞介素1预处理可减少暴露于高氧环境下大鼠的肺氧化型谷胱甘肽蓄积、肺损伤及死亡率。
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暴露于高压氧会诱导大鼠巨噬细胞分泌肿瘤坏死因子-α(TNF-α)。

Exposure to hyperbaric oxygen induces tumour necrosis factor-alpha (TNF-alpha) secretion from rat macrophages.

作者信息

Lahat N, Bitterman H, Yaniv N, Kinarty A, Bitterman N

机构信息

Israel Naval Medical Institute, Immunological Research Unit, Haifa, Israel.

出版信息

Clin Exp Immunol. 1995 Dec;102(3):655-9. doi: 10.1111/j.1365-2249.1995.tb03867.x.

DOI:10.1111/j.1365-2249.1995.tb03867.x
PMID:8536387
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1553383/
Abstract

We investigated the secretion of TNF-alpha by monocytes and macrophages derived from the peripheral blood, spleen, and lungs after a single exposure to a therapeutic profile of hyperbaric oxygen (HBO). Rats were exposed for 90 min to either 100% oxygen at 0.28 MPa (2.8 atmospheres absolute) or air. Immediately after exposure, mononuclear cells were isolated from blood, spleen, and lungs and cultured for 18 h. The secretion of TNF-alpha from the cultured monocytes/macrophages was determined with and without stimulation with lipopolysaccharide (LPS). Exposure to hyperbaric oxygen induced a significant increase in the spontaneous ex vivo secretion of TNF-alpha (without LPS) by mononuclear cells from the blood, spleen, and lung (P < 0.05 from air controls). Stimulation with LPS after exposure to HBO induced a significant increase in TNF-alpha secretion by lung and spleen macrophages compared with air controls (P < 0.05). However, absolute TNF-alpha levels were not significantly higher than those achieved 'spontaneously' in macrophages exposed to HBO without LPS. Stimulation with LPS induced a marked increase in secretion of TNF-alpha from blood monocytes after exposure to air, but not after exposure to HBO. These results provide evidence in support of a role played by TNF-alpha in mediating HBO effects on different tissues and their immune responses.

摘要

我们研究了单次暴露于高压氧(HBO)治疗参数后,外周血、脾脏和肺脏来源的单核细胞和巨噬细胞中肿瘤坏死因子-α(TNF-α)的分泌情况。将大鼠暴露于0.28 MPa(2.8个绝对大气压)的100%氧气或空气中90分钟。暴露后立即从血液、脾脏和肺脏中分离单核细胞并培养18小时。在有或无脂多糖(LPS)刺激的情况下,测定培养的单核细胞/巨噬细胞中TNF-α的分泌。暴露于高压氧会导致血液、脾脏和肺脏的单核细胞在体外自发分泌TNF-α(无LPS)显著增加(与空气对照组相比,P < 0.05)。暴露于HBO后用LPS刺激,与空气对照组相比,肺脏和脾脏巨噬细胞中TNF-α的分泌显著增加(P < 0.05)。然而,TNF-α的绝对水平并不显著高于未用LPS处理的暴露于HBO的巨噬细胞“自发”达到的水平。用LPS刺激会使暴露于空气后的血液单核细胞中TNF-α的分泌显著增加,但暴露于HBO后则不会。这些结果为TNF-α在介导HBO对不同组织及其免疫反应的作用提供了证据支持。