کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5831729 | 1559752 | 2016 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Administration of SB239063, a potent p38 MAPK inhibitor, alleviates acute lung injury induced by intestinal ischemia reperfusion in rats associated with AQP4 downregulation
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کلمات کلیدی
AQPsPVDFTNF-alphaIntestinal ischemia reperfusionAquaporinsIL-1βAQP4NIHMAPK - MAPKp38 MAPK - P38 MAPKAcute lung injury - آسیب ریه حادaquaporin 4 - آکوپورین 4Sprague-Dawley - اسپراگ داولیAli - اماintestinal ischemia-reperfusion - ایسکمی روده ای-رپرفیوژنtumor necrosis factor-alpha - تومور نکروز عامل آلفاSMA - دبیرستانpolyvinylidene difluoride - دی فلوئورید پلی وینیلیدینImmunofluorescent staining - رنگ آمیزی ایمونوفلورسنتsuperior mesenteric artery - سرخرگ روده بندی بالایی، شریان مزانتر فوقانیCoeliac artery - شریان سلیاکphosphorylated - فسفریلید شدهNational Institutes of Health - مؤسسات ملی بهداشتRat - موش صحراییhematoxylin-eosin - هماتوکسیلین ائوزینWestern blot - وسترن بلاتmitogen activated protein kinase - پروتئین کیناز فعال Mitogen فعال است
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Acute lung injury (ALI), induced by intestinal ischemia reperfusion (II/R) injury, is characterized by pulmonary edema and inflammation. Aquaporin 4 (AQP4), has been pointed out recently involving in edema development. Previous studies have shown that p38 mitogen activated protein kinase (MAPK) activation resulted in lung inflammation, while p38 MAPK inhibitor can alleviate the pathology injury of lung tissue. However, the regulated mechanism of p38 MAPK in ALI induced by II/R is unclear. In this study, we established II/R rats' model by clamping the superior mesenteric artery (SMA) and coeliac artery (CA) for 40Â min and subsequent reperfusion for 16Â h, 24Â h, 48Â h. Subsequently, SB239063, a specific inhibitor of the activity of p38 MAPK, was injected (10Â mg/kg) intraperitoneally 60Â min before the operation. The severity of ALI was determined by histology analysis (HE staining and ALI scoring) and lung edema (lung wet/dry weight ratio) assessment. Western blot (WB) was applied to detect the expression level of AQP4 and phosphorylated (P)-p38 MAPK, and the localization of AQP4 was detected by immunofluorescent staining (IF). We found that AQP4 could express in the lung tissue. II/R could significantly induce lung injury, confirmed by lung injury scores and lung wet/dry weight ratios. The level of P-p38 MAPK and AQP4 were largely up-regulated in lung tissues. Moreover, inhibition of p38 MAPK activity could effectively down-regulate AQP4 expression and diminish the severity of II/R-induced ALI. These novel findings suggest that inhibition of p38 MAPK function should be a potential strategy for the prevention or treatment of ALI, by targeting AQP4 in future clinic trial.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: International Immunopharmacology - Volume 38, September 2016, Pages 54-60
Journal: International Immunopharmacology - Volume 38, September 2016, Pages 54-60
نویسندگان
Liu-Lin Xiong, Yan Tan, Hong-Yu Ma, Ping Dai, Yan-Xia Qin, Rui-ai Yang, Yan-Yan Xu, Zheng Deng, Wei Zhao, Qin-Jie Xia, Ting-Hua Wang, Yun-Hui Zhang,