Protective Effects of Neural Crest-Derived Stem Cell-Conditioned Media against Ischemia-Reperfusion-Induced Lung Injury in Rats

被引:0
|
作者
Chung-Kan Peng
Shu-Yu Wu
Shih-En Tang
Min-Hui Li
Shih-Shiuan Lin
Shi-Jye Chu
Kun-Lun Huang
机构
[1] Tri-Service General Hospital,Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine
[2] National Defense Medical Center,Department of Physical Medicine and Rehabilitation
[3] Institute of Aerospace and Undersea Medicine,Division of Rheumatology, Immunology and Allergy, Department of Internal Medicine
[4] National Defense Medical Center,undefined
[5] Kaohsiung Veterans General Hospital,undefined
[6] Tri-Service General Hospital,undefined
[7] National Defense Medical Center,undefined
[8] Institute of Aerospace and Undersea Medicine,undefined
[9] National Defense Medical Center,undefined
来源
Inflammation | 2017年 / 40卷
关键词
acute lung injury; ischemia-reperfusion; neural crest stem cell; conditioned media;
D O I
暂无
中图分类号
学科分类号
摘要
Current treatments for ischemia-reperfusion (IR)-induced acute lung injury are limited. Mesenchymal stem cell-conditioned medium (CM) has been reported to attenuate lung injury. Neural crest stem cells (NCSCs), a type of multipotent stem cells, are more easily obtained than mesenchymal stem cells. We hypothesize that NCSC-CM has anti-inflammatory properties that could protect against IR-induced lung injury in rats. In this study, NCSC-CM was derived from rat NCSCs. Typical acute lung injury was induced by 30-min ischemia followed by 90-min reperfusion in adult male Sprague–Dawley rats. Bronchoalveolar lavage fluid (BALF) and lung tissues were collected to analyze the degree of lung injury after the experiment. NCSC-CM was administered before ischemia and after reperfusion. NCSC-CM treatment significantly attenuated IR-induced lung edema, as indicated by decreases in pulmonary vascular permeability, lung weight gain, wet to dry weight ratio, lung weight to body weight ratio, pulmonary arterial pressure, and protein level in BALF. The levels of tumor necrosis factor-α and interleukin-6 in the BALF were also significantly decreased. Additionally, NCSC-CM improved lung pathology and neutrophil infiltration in the lung tissue, and significantly suppressed nuclear factor (NF)-κB activity and IκB-α degradation in the lung. However, heating NCSC-CM eliminated these protective effects. Our experiment demonstrates that NCSC-CM treatment decreases IR-induced acute lung injury and that the protective mechanism may be attributable to the inhibition of NF-κB activation and the inflammatory response. Therefore, NCSC-CM may be a novel approach for treating IR-induced lung injury.
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页码:1532 / 1542
页数:10
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