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学科主题: 临床医学
题名:
Melatonin prevents lung injury induced by hepatic ischemia-reperfusion through anti-inflammatory and anti-apoptosis effects
作者: Zhou, Li1,2; Zhao, Dong3; An, Haiyan3; Zhang, Hong3; Jiang, Chunling1,2; Yang, Baxian3
关键词: Melatonin ; Acute lung injury ; Hepatic ischemia/reperfusion ; MAPK signaling ; NF-kappa B signaling ; Nrf2 signaling
刊名: INTERNATIONAL IMMUNOPHARMACOLOGY
发表日期: 2015-12-01
DOI: 10.1016/j.intimp.2015.10.012
卷: 29, 期:2, 页:462-467
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Immunology ; Pharmacology & Pharmacy
研究领域[WOS]: Immunology ; Pharmacology & Pharmacy
关键词[WOS]: LIVER ISCHEMIA/REPERFUSION INJURY ; KAPPA-B ACTIVATION ; PROTECTS ; TRANSPLANTATION ; COMPLICATIONS ; INFLAMMATION ; ANTIOXIDANT ; INHIBITION ; AUTOPHAGY ; RATS
英文摘要:

Melatonin is a free radical scavenger and broad-spectrum antioxidant with immunomodulatory effects. The objective of the study is to investigate the effects of melatonin in hepatic ischemia/reperfusion (I/R) induced lung injury and explore its underlying mechanisms. Hepatic I/R injury was induced via portal vein and hepatic artery occlusion for 30 min followed by 3-h reperfusion. Male Sprague-Dawley rats were divided into three groups: sham, I/R + Vehicle and I/R + melatonin. Melatonin (10 mg/kg) or vehicle was injected intravenously 15 min before ischemia and 10 min before reperfusion. The histology of the liver and lung, plasma aminotransferase and cytokine secretion, and apoptosis in the lung were evaluated. The phosphorylation of JNK, p38, and NF-B and Nrf2 nuclear translocation in the lung was examined by Western blotting. We found that melatonin administration significantly attenuated hepatic I/R induced lung injury in rats. Melatonin inhibited the pro-inflammatory responses and enhanced antioxidative responses. Melatonin alleviated pathological changes of the lung and liver, and inhibited apoptosis of cells in the lung. Phosphotylation of JNK, p38 and NF-B and Nrf2 nuclear translocation was increased significantly in the lung by hepatic I/R. Melatonin administration inhibited the activation of JNK, p38, and NF-B, however, melatonin further enhanced Nrf2 activation. We conclude that melatonin exerts a protective effect in hepatic I/R induced lung injury by attenuating the pro-inflammatory responses, inhibiting cell apoptosis, which was mediated in part through JNK, p38 MAPK, NF-B and Nrf2 signaling pathways. Melatonin may be a promising therapeutic strategy for hepatic I/R induced lung injury. (C) 2015 Elsevier B.V. All rights reserved.

语种: 英语
WOS记录号: WOS:000366764800029
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/61556
Appears in Collections:北京大学第二临床医学院_麻醉科_期刊论文

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作者单位: 1.West China Hosp, Dept Anesthesiol, Chengdu 610041, Peoples R China
2.West China Hosp, Translat Neurosci Ctr, Chengdu 610041, Peoples R China
3.Peking Univ, Peoples Hosp, Dept Anesthesiol, Beijing 100044, Peoples R China

Recommended Citation:
Zhou, Li,Zhao, Dong,An, Haiyan,et al. Melatonin prevents lung injury induced by hepatic ischemia-reperfusion through anti-inflammatory and anti-apoptosis effects[J]. INTERNATIONAL IMMUNOPHARMACOLOGY,2015,29(2):462-467.
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