• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

p38丝裂原活化蛋白激酶在巨噬细胞介导的炎症反应中的功能作用。

Functional roles of p38 mitogen-activated protein kinase in macrophage-mediated inflammatory responses.

作者信息

Yang Yanyan, Kim Seung Cheol, Yu Tao, Yi Young-Su, Rhee Man Hee, Sung Gi-Ho, Yoo Byong Chul, Cho Jae Youl

机构信息

Department of Genetic Engineering, Sungkyunkwan University, Suwon 440-746, Republic of Korea.

Division of Gynecologic Oncology Department of Obstetrics and Gynecology, Ewha Womans University Mokdong Hospital College of Medicine, Ewha Womans University, Seoul 158-710, Republic of Korea.

出版信息

Mediators Inflamm. 2014;2014:352371. doi: 10.1155/2014/352371. Epub 2014 Mar 20.

DOI:10.1155/2014/352371
PMID:24771982
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3977509/
Abstract

Inflammation is a natural host defensive process that is largely regulated by macrophages during the innate immune response. Mitogen-activated protein kinases (MAPKs) are proline-directed serine and threonine protein kinases that regulate many physiological and pathophysiological cell responses. p38 MAPKs are key MAPKs involved in the production of inflammatory mediators, including tumor necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2). p38 MAPK signaling plays an essential role in regulating cellular processes, especially inflammation. In this paper, we summarize the characteristics of p38 signaling in macrophage-mediated inflammation. In addition, we discuss the potential of using inhibitors targeting p38 expression in macrophages to treat inflammatory diseases.

摘要

炎症是一种天然的宿主防御过程，在固有免疫反应期间主要由巨噬细胞调节。丝裂原活化蛋白激酶（MAPKs）是脯氨酸定向的丝氨酸和苏氨酸蛋白激酶，可调节许多生理和病理生理细胞反应。p38 MAPKs是参与炎症介质产生的关键MAPKs，包括肿瘤坏死因子-α（TNF-α）和环氧化酶-2（COX-2）。p38 MAPK信号传导在调节细胞过程，尤其是炎症中起重要作用。在本文中，我们总结了巨噬细胞介导的炎症中p38信号传导的特征。此外，我们讨论了使用靶向巨噬细胞中p38表达的抑制剂治疗炎症性疾病的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1f7/3977509/5041b34ec546/MI2014-352371.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1f7/3977509/18c58438c56a/MI2014-352371.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1f7/3977509/5041b34ec546/MI2014-352371.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1f7/3977509/18c58438c56a/MI2014-352371.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1f7/3977509/5041b34ec546/MI2014-352371.002.jpg

相似文献

1
Functional roles of p38 mitogen-activated protein kinase in macrophage-mediated inflammatory responses.p38丝裂原活化蛋白激酶在巨噬细胞介导的炎症反应中的功能作用。
Mediators Inflamm. 2014;2014:352371. doi: 10.1155/2014/352371. Epub 2014 Mar 20.
2
Strong inhibition of TNF-alpha production and inhibition of IL-8 and COX-2 mRNA expression in monocyte-derived macrophages by RWJ 67657, a p38 mitogen-activated protein kinase (MAPK) inhibitor.p38丝裂原活化蛋白激酶（MAPK）抑制剂RWJ 67657对单核细胞衍生巨噬细胞中TNF-α的产生具有强烈抑制作用，并抑制IL-8和COX-2 mRNA的表达。
Arthritis Res Ther. 2004;6(4):R384-92. doi: 10.1186/ar1204. Epub 2004 Jun 21.
3
Thioredoxin-interacting protein-derived peptide (TN13) inhibits LPS-induced inflammation by inhibiting p38 MAPK signaling.硫氧还蛋白相互作用蛋白衍生肽（TN13）通过抑制 p38 MAPK 信号通路抑制 LPS 诱导的炎症。
Biochem Biophys Res Commun. 2018 Dec 9;507(1-4):489-495. doi: 10.1016/j.bbrc.2018.11.069. Epub 2018 Nov 16.
4
The role of mitogen-activated protein kinase phosphatase-1 in the response of alveolar macrophages to lipopolysaccharide: attenuation of proinflammatory cytokine biosynthesis via feedback control of p38.丝裂原活化蛋白激酶磷酸酶-1在肺泡巨噬细胞对脂多糖反应中的作用：通过对p38的反馈控制减弱促炎细胞因子生物合成
J Biol Chem. 2005 Mar 4;280(9):8101-8. doi: 10.1074/jbc.M411760200. Epub 2004 Dec 8.
5
Anti-inflammatory effect of Sosihotang via inhibition of nuclear factor-κB and mitogen-activated protein kinases signaling pathways in lipopolysaccharide-stimulated RAW 264.7 macrophage cells.四逆汤通过抑制核因子-κB 和丝裂原活化蛋白激酶信号通路对脂多糖刺激的 RAW 264.7 巨噬细胞的抗炎作用。
Food Chem Toxicol. 2013 Mar;53:343-51. doi: 10.1016/j.fct.2012.12.006. Epub 2012 Dec 12.
6
DBM1285 suppresses tumor necrosis factor alpha production by blocking p38 mitogen-activated protein kinase/mitogen-activated protein kinase-activated protein kinase 2 signaling pathway.DBM1285 通过阻断 p38 丝裂原活化蛋白激酶/丝裂原活化蛋白激酶激活蛋白激酶 2 信号通路抑制肿瘤坏死因子 α 的产生。
J Pharmacol Exp Ther. 2010 Aug;334(2):657-64. doi: 10.1124/jpet.109.161687. Epub 2010 Apr 28.
7
Mycobacteria-induced TNF-alpha and IL-10 formation by human macrophages is differentially regulated at the level of mitogen-activated protein kinase activity.分枝杆菌诱导人巨噬细胞产生肿瘤坏死因子-α和白细胞介素-10的过程在丝裂原活化蛋白激酶活性水平受到不同调控。
J Immunol. 2001 Sep 15;167(6):3339-45. doi: 10.4049/jimmunol.167.6.3339.
8
Role of MAP kinase pathways in mediating IL-6 production in human primary mesangial and proximal tubular cells.丝裂原活化蛋白激酶（MAP）通路在介导人原代系膜细胞和近端肾小管细胞产生白细胞介素-6中的作用。
Kidney Int. 1999 Oct;56(4):1366-77. doi: 10.1046/j.1523-1755.1999.00664.x.
9
Enhanced phosphorylation of MAPKs by NE promotes TNF-α production by macrophage through α adrenergic receptor.NE 通过α肾上腺素能受体增强 MAPKs 的磷酸化，促进巨噬细胞产生 TNF-α。
Inflammation. 2012 Apr;35(2):527-34. doi: 10.1007/s10753-011-9342-4.
10
Possible pathophysiological roles of mitogen-activated protein kinases (MAPKs) in endometriosis.丝裂原活化蛋白激酶（MAPKs）在子宫内膜异位症中可能的病理生理作用。
Am J Reprod Immunol. 2004 Nov;52(5):306-11. doi: 10.1111/j.1600-0897.2004.00231.x.

引用本文的文献

1
Geniposide Mitigates Insulin Resistance and Hepatic Fibrosis via Insulin Signaling Pathway.京尼平苷通过胰岛素信号通路减轻胰岛素抵抗和肝纤维化。
Int J Mol Sci. 2025 Aug 21;26(16):8079. doi: 10.3390/ijms26168079.
2
Ziziphus nummularia extract attenuates inflammatory markers in RAW 264.7 macrophages.枣叶提取物可减轻RAW 264.7巨噬细胞中的炎症标志物。
Sci Rep. 2025 Jul 20;15(1):26362. doi: 10.1038/s41598-025-07273-2.
3
Spatially-distinct programming of macrophage diversity within the granulomas of infected nonhuman primates.感染非人灵长类动物肉芽肿内巨噬细胞多样性的空间特异性编程。

本文引用的文献

1
Effects of Korean Red Ginseng extract on tissue plasminogen activator and plasminogen activator inhibitor-1 expression in cultured rat primary astrocytes.红参提取物对培养的大鼠原代星形胶质细胞组织型纤溶酶原激活物和纤溶酶原激活物抑制剂-1 表达的影响。
J Ginseng Res. 2013 Oct;37(4):401-12. doi: 10.5142/jgr.2013.37.401.
2
Kalopanaxsaponin B Ameliorates TNBS-Induced Colitis in Mice.高丽参皂苷 B 可改善三硝基苯磺酸诱导的小鼠结肠炎。
Biomol Ther (Seoul). 2012 Sep;20(5):457-62. doi: 10.4062/biomolther.2012.20.5.457.
3
Immunomodulation of Fungal β-Glucan in Host Defense Signaling by Dectin-1.
bioRxiv. 2025 Jun 17:2025.06.12.659348. doi: 10.1101/2025.06.12.659348.
4
Anti-Inflammatory Activity and Mechanism of Stearic Acid Extract From Purslane.马齿苋硬脂酸提取物的抗炎活性及作用机制
Food Sci Nutr. 2025 Jul 10;13(7):e70596. doi: 10.1002/fsn3.70596. eCollection 2025 Jul.
5
A novel modulator of IL-6R prevents inflammation-induced preterm birth and improves newborn outcome.一种新型白细胞介素-6受体调节剂可预防炎症诱导的早产并改善新生儿结局。
EMBO Mol Med. 2025 Jul 3. doi: 10.1038/s44321-025-00257-9.
6
Beyond the hype: a comprehensive exploration of CBD's biological impacts and mechanisms of action.超越炒作：对CBD的生物学影响和作用机制的全面探索
J Cannabis Res. 2025 May 11;7(1):24. doi: 10.1186/s42238-025-00274-y.
7
Dexamethasone-Induced MerTK M2c Macrophages Exhibit a Preference for Downregulated Gene Expression Profiles.地塞米松诱导的MerTK M2c巨噬细胞表现出对下调基因表达谱的偏好。
J Genomics. 2025 Mar 31;13:24-39. doi: 10.7150/jgen.108648. eCollection 2025.
8
The relationship mammalian p38 with human health and its homolog Hog1 in response to environmental stresses in .哺乳动物p38与其同源物Hog1在应对环境压力时与人类健康的关系。 （注：原英文文本表述不太完整规范，翻译后的中文也稍显拗口，但尽量忠实于原文进行了翻译）
Front Cell Dev Biol. 2025 Mar 10;13:1522294. doi: 10.3389/fcell.2025.1522294. eCollection 2025.
9
Inhibitory effects of AptaminC320 targeting vitamin C on LPS-induced inflammation in RAW264.7 cells.靶向维生素C的AptaminC320对RAW264.7细胞中脂多糖诱导的炎症的抑制作用。
Biochem Biophys Rep. 2025 Feb 18;41:101951. doi: 10.1016/j.bbrep.2025.101951. eCollection 2025 Mar.
10
Cisplatin-induced oxidative stress, apoptosis, and pro-inflammatory responses in chondrocytes through modulating LOX-1.顺铂通过调节凝集素样氧化型低密度脂蛋白受体1（LOX-1）诱导软骨细胞产生氧化应激、凋亡和促炎反应。
J Orthop Surg Res. 2025 Feb 26;20(1):206. doi: 10.1186/s13018-025-05602-9.
通过脱屑素-1对真菌β-葡聚糖在宿主防御信号传导中的免疫调节作用
Biomol Ther (Seoul). 2012 Sep;20(5):433-45. doi: 10.4062/biomolther.2012.20.5.433.
4
Floridoside suppresses pro-inflammatory responses by blocking MAPK signaling in activated microglia.弗洛里多苷通过阻断活化小胶质细胞中的 MAPK 信号通路来抑制促炎反应。
BMB Rep. 2013 Aug;46(8):398-403. doi: 10.5483/bmbrep.2013.46.8.237.
5
Activation of p38 signaling increases utrophin A expression in skeletal muscle via the RNA-binding protein KSRP and inhibition of AU-rich element-mediated mRNA decay: implications for novel DMD therapeutics.p38 信号通路的激活通过 RNA 结合蛋白 KSRP 增加骨骼肌中的 utrophin A 表达，并抑制 AU 富含元件介导的 mRNA 降解：对新型 DMD 治疗的意义。
Hum Mol Genet. 2013 Aug 1;22(15):3093-111. doi: 10.1093/hmg/ddt165. Epub 2013 Apr 10.
6
Efficacy and safety of the oral p38 inhibitor PH-797804 in chronic obstructive pulmonary disease: a randomised clinical trial.口服 p38 抑制剂 PH-797804 治疗慢性阻塞性肺疾病的疗效和安全性：一项随机临床试验。
Thorax. 2013 Aug;68(8):738-45. doi: 10.1136/thoraxjnl-2012-202744. Epub 2013 Mar 28.
7
Inflammation alters the expression of DMT1, FPN1 and hepcidin, and it causes iron accumulation in central nervous system cells.炎症改变了 DMT1、FPN1 和铁调素的表达，导致铁在中枢神经系统细胞中积累。
J Neurochem. 2013 Aug;126(4):541-9. doi: 10.1111/jnc.12244. Epub 2013 Apr 3.
8
Deficiency in p38β MAPK fails to inhibit cytokine production or protect neurons against inflammatory insult in in vitro and in vivo mouse models.p38β MAPK 缺陷不能抑制细胞因子产生或保护神经元免受体内外小鼠模型炎症损伤。
PLoS One. 2013;8(2):e56852. doi: 10.1371/journal.pone.0056852. Epub 2013 Feb 15.
9
AP-1 pathway-targeted inhibition of inflammatory responses in LPS-treated macrophages and EtOH/HCl-treated stomach by Archidendron clypearia methanol extract.阿丁枫甲醇提取物对 LPS 处理的巨噬细胞和 EtOH/HCl 处理的胃的 AP-1 通路靶向抑制炎症反应。
J Ethnopharmacol. 2013 Mar 27;146(2):637-44. doi: 10.1016/j.jep.2013.01.034. Epub 2013 Feb 8.
10
The pivotal role of TBK1 in inflammatory responses mediated by macrophages.TBK1 在巨噬细胞介导的炎症反应中的关键作用。
Mediators Inflamm. 2012;2012:979105. doi: 10.1155/2012/979105. Epub 2012 Dec 6.