摘要
背景:抵抗素样分子-α(RELMα)在炎症中有多种调控机制,但在急性重症胰腺炎(SAP)和急性胰腺炎肺损伤(APALI)中的作用仍不清楚。 方法:SAP在鼠中诱发。RELMα蛋白表达在鼠肺组织中检测来决定APALI和RELMα.的关系。为了研究RELMα过表达或压低APALI的影响,大鼠在SAP诱导前静脉注射腺病毒载体。肺和胰腺样品在诱导后16小时采集。在检测RELMα蛋白水平后,胰腺损伤和肺部损伤严重程度从组织学上评价,血清和组织炎性介质水平经过测定。TUNEL测定和免疫荧光用来估计RELMα抑制的SAP鼠的肺组织中肺组织细胞凋亡和内皮屏障的完整性。 结果:RELMα表达在APALI中显著上调并和肺损伤指数有关。RELMα过表达加强细胞炎症因子包括白细胞介素(IL)-1β, IL-6, IL-8, 肿瘤坏死因子-α,和血清C-反应蛋白的释放;炎症介质磷酸化(p)-AKT, p-P65, p-P38有丝分裂原活化蛋白激酶的释放,对细胞外信号调节激酶和细胞内粘附分子-1的释放;和肺损伤。RELMα抑制有相反影响。另外,RELMα抑制提高了SAP鼠肺组织中增殖细胞核抗原,Bcl-2,zonal occluding-1,Claudin-1的表达。 结论:RELMα在SAP中与肺损伤严重程度有关。RELMα通过增加炎症因子释放来增强炎症活动。
关键词: RELMα
Current Molecular Medicine
Title:Resistin-Like Molecule-α Causes Lung Injury in Rats with Acute Pancreatitis by Activating the PI-3K/Akt-NF-κB Pathway and Promoting Inflammatory Cytokine Release
Volume: 16 Issue: 7
Author(s): W.-Y. Wang, Y. Chen, X. Su, D. Tang, Q.-W. Ben, W.-Y. Yao, P. Chen, Y.-Z. Yuan
Affiliation:
关键词: RELMα
摘要: Background: Resistin-like molecule-α (RELMα) has diverse regulatory functions in inflammation, but its role in severe acute pancreatitis (SAP) and acute pancreatitis associated lung injury (APALI) remains unclear.
Methods: SAP was induced in rats. RELMα protein expression was detected in lung tissue of rats to determine the relationship between APALI and RELMα. To investigate the effect of RELMα overexpression or knockdown on APALI, rats were given an intravenous injection of adenovirus vector before SAP induction. Lung and pancreatic samples were harvested 16 h after induction. After detection of RELMα protein levels, the severity of pancreatic and pulmonary injury was scored histologically, and serum and tissue levels of inflammatory mediators were measured. TUNEL assay and immunofluorescence were used to estimate pulmonary apoptosis and endothelial barrier integrity in lung tissue of SAP rats with RELMα knockdown.
Results: RELMα expression was significantly up-regulated in APALI and was related to the lung injury index. RELMα overexpression aggravated the release of inflammatory cytokines including interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor-α, and serum C-reaction protein; the expression of inflammatory mediators phosphorylated (p)-AKT, p-P65, p-P38 mitogen activated protein kinase, p-extracellular regulated kinase, and intracellular adhesion molecule-1; and lung injury. RELMα knockdown had opposite effects. In addition, RELMα knockdown improved expression of proliferative cellular nuclear antigen, Bcl-2, zonal occluding-1 and Claudin-1 in lung tissue of SAP rats.
Conclusion: RELMα is associated with lung injury severity in SAP. RELMα augments inflammatory activity by increasing inflammatory cytokine release.
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W.-Y. Wang, Y. Chen, X. Su, D. Tang, Q.-W. Ben, W.-Y. Yao, P. Chen, Y.-Z. Yuan , Resistin-Like Molecule-α Causes Lung Injury in Rats with Acute Pancreatitis by Activating the PI-3K/Akt-NF-κB Pathway and Promoting Inflammatory Cytokine Release, Current Molecular Medicine 2016; 16 (7) . https://dx.doi.org/10.2174/1566524016666160802145700
DOI https://dx.doi.org/10.2174/1566524016666160802145700 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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