کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10143571 | 1646183 | 2018 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
LipoxinA4 attenuates acute pancreatitis-associated acute lung injury by regulating AQP-5 and MMP-9 expression, anti-apoptosis and PKC/SSeCKS-mediated F-actin activation
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کلمات کلیدی
LPSLXSSSeCKSpulmonary microvascular endothelial cellLXA4AQPsMODSSIRSPKCAquaporinsHRPMMP-9Small interfering RNA - RNA تداخل کوچکsiRNA - siRNAAcute lung injury - آسیب ریه حادAli - اماHuman pulmonary microvascular endothelial cells - سلولهای اندوتلیال میکروواسکولار ریه انسانMultiple organ dysfunction syndrome - سندرم اختلال عملکرد چندگانهSystemic inflammatory response syndrome - سندرم پاسخ سیستماتیک التهابیlipopolysaccharide - لیپوپلی ساکاریدLipoxins - لیپوکسین هاlipoxin A4 - لیپوکین A4matrix metalloproteinases-9 - ماتریکس متالوپروتئیناز -9Acute pancreatitis - پانکراتیت حادHorseradish peroxidase - پراکسیداز هوررادیشProtein kinase C - پروتئین کیناز سی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی مولکولی
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چکیده انگلیسی
An essential component of acute pancreatitis(AP)-induced acute lung injury(ALI) is the inflammation that is part of the body's systemic inflammatory response to a variety of systemic stimuli. Lipoxins(LXs) are considered important endogenous lipids that mediate the resolution of inflammation. In previous studies, we found that Lipoxin A4 (LXA4) reduced AP-induced pulmonary oedema and TNF-α production in lung. However, the underlying mechanism remains unclear. Due to the above studies, we investigated the aquaporin, matrix metalloprotein, apoptosis and PKC/SSeCKS signal pathway in cellular and animal models of AP-associated lung injury following LXA4 intervention. In this study, we first proved LXA4 could effectively promote F-actin reconstruction and regulate its expression in pulmonary microvascular endothelial cells both in vivo and vitro via suppressing PKC/SSeCKS signalling pathway. Next, we found that LXA4 attenuated cell growth inhibition and apoptosis in lung tissues of AP-ALI mice and HPMECs. Additionally, we demonstrated that LXA4 could regulate the expression of AQP-5 and MMP-9 to stabilize the permeability of pulmonary microvascular endothelial cell. In summary, our results suggest that the anti-inï¬ammatory eï¬ ;ects of LXA4 may be due to the inhibition of both the PKC/SSeCKS pathway and apoptosis to reduce alveolar fluid exudation and to the regulation of AQP-5 and MMP-9 expression to maintain the clearance of alveolar fluid. Thus, LXA4 is capable of exerting protective eï¬ ;ects on AP-induced ALI.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Immunology - Volume 103, November 2018, Pages 78-88
Journal: Molecular Immunology - Volume 103, November 2018, Pages 78-88
نویسندگان
Zhehao Shi, Wen Ye, Jiecheng Zhang, Fan Zhang, Dinglai Yu, Huajun Yu, Bicheng Chen, Mengtao Zhou, Hongwei Sun,