کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8286358 | 1535832 | 2018 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Pomegranate prevents binge alcohol-induced gut leakiness and hepatic inflammation by suppressing oxidative and nitrative stress
ترجمه فارسی عنوان
انار از مهار استرس اکسیداتیو و نیترات جلوگیری از نشتگی روده ناشی از الکل و التهاب کبدی را از بین می برد
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کلمات کلیدی
POMiNOSPDITEERTLR4Binge alcoholCMZCYP2E1KO miceAdherent junctionJnkUrolithin ALPSelF2αPTMprotein kinase-like endoplasmic reticulum kinasec-Jun N-terminal protein kinase - C-Jun N-terminal protein kinaseBAC - LACROS - ROSALD - آدرنولکودیستروفیTight junction - اتصال تنگNitroxidative stress - استرس نیتروکسیدیpost-translational modification - اصلاح post-translationalEllagic acid - الاجیک اسیدPomegranate - انارalcoholic liver disease - بیماری کبدی الکلیImmunoprecipitation - تخریب ایمنیinducible nitric oxide synthase - سنتاز اکسید نیتریک القاییendoplasmic reticulum - شبکه آندوپلاسمی Blood alcohol concentration - غلظت الکل خونlipopolysaccharide - لیپوپلی ساکاریدTrans-epithelial electrical resistance - مقاومت الکتریکی Trans-epithelialKnock-out mice - موش نابود شدهKnock-in mice - موش نابود شدهprotein disulfide isomerase - پروتئین دیسولفید ایزومرازPERK - پرکChlormethiazole - کلرومتیاازولReactive oxygen species - گونههای فعال اکسیژنToll-like receptor-4 - گیرنده سفارشی -4
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
چکیده انگلیسی
Alcoholic liver disease (ALD) is a major chronic liver disease worldwide and can range from simple steatosis, inflammation to fibrosis/cirrhosis possibly through leaky gut and systemic endotoxemia. We investigated whether pomegranate (POM) protects against binge alcohol-induced gut leakiness, endotoxemia, and inflammatory liver damage. After POM pretreatment for 10 days, rats were exposed to 3 oral doses of binge alcohol (5â¯g/kg/dose) or dextrose (as control) at 12-h intervals. Binge alcohol exposure induced leaky gut with significantly elevated plasma endotoxin and inflammatory fatty liver by increasing the levels of oxidative and nitrative stress marker proteins such as ethanol-inducible CYP2E1, inducible nitric oxide synthase, and nitrated proteins in the small intestine and liver. POM pretreatment significantly reduced the alcohol-induced gut barrier dysfunction, plasma endotoxin and inflammatory liver disease by inhibiting the elevated oxidative and nitrative stress marker proteins. POM pretreatment significantly restored the levels of intestinal tight junction (TJ) proteins such as ZO-1, occludin, claudin-1, and claundin-3 markedly diminished after alcohol-exposure. In addition, the levels of gut adherent junction (AJ) proteins (e.g., β-catenin and E-cadherin) and desmosome plakoglobin along with associated protein α-tubulin were clearly decreased in binge alcohol-exposed rats but restored to basal levels in POM-pretreated rats. Immunoprecipitation followed by immunoblot analyses revealed that intestinal claudin-1 protein was nitrated and ubiquitinated in alcohol-exposed rats, whereas these modifications were significantly blocked by POM pretreatment. These results showed for the first time that POM can prevent alcohol-induced gut leakiness and inflammatory liver injury by suppressing oxidative and nitrative stress.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Redox Biology - Volume 18, September 2018, Pages 266-278
Journal: Redox Biology - Volume 18, September 2018, Pages 266-278
نویسندگان
Young-Eun Cho, Byoung-Joon Song,