کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2598360 1562617 2016 11 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Mainstream cigarette smoke accelerates the progression of nonalcoholic steatohepatitis by modulating Kupffer cell-mediated hepatocellular apoptosis in adolescent mice
ترجمه فارسی عنوان
دود سیگار جریان اصلی باعث تسریع پیشرفت استئاتوهپاتیت غیرالکلی با تعدیل هآپوپتوز پاتوسلولار با واسطه سلول کوپفر در موش نوجوان می شود
کلمات کلیدی
بیماری غیرالکلی کبد چرب؛ سلول های بنیادی جریان اصلی دود سیگار . استئاتوهپاتیت غیرالکلی. کمبود کولین به همراه چربی بالا؛ عصاره دود سیگار؛ سلول های KCS، کوپفر؛ SSCS، جریان سمت CS؛ NAS، NAFLD
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
چکیده انگلیسی


• Mainstream cigarette smoke accelerates the progression of nonalcoholic steatohepatitis.
• Mainstream cigarette smoke activates Kupffer cells to release inflammatory cytokines and oxidative stress.
• Mainstream cigarette smoke induces hepatocellular apoptosis.

Cigarette smoking in adolescents is considered to be a major cause of preventable morbidity and mortality. The purpose of this study is to investigate the role of mainstream cigarette smoke (MSCS) on the progression of nonalcoholic steatohepatitis in adolescents. Three-week-old C57BL/6 mice were fed either a methionine and choline-deficient plus high fat (MCDHF) diet for 6 weeks. Each group was exposed to MSCS (300, 600 ug/L) or fresh air for 2 h per day during the first 3 weeks of MCDHF diet feeding. MSCS increased MCDHF diet-induced NASH by increasing serum ALT/AST levels, steatosis, inflammation, and fibrosis. Furthermore, MSCS was associated with the degree of oxidative stress and hepatocellular apoptosis in NASH mice, but not prominent in controls. In vitro, cigarette smoke extract (CSE) activated Kupffer cells (KCs) to release inflammatory cytokines and oxidative stress, which induced hepatocellular apoptosis. In conclusion, MSCS exposure accelerates the progression and severity of NASH by modulating KC-mediated hepatocellular apoptosis. Our results support the regulation of CS in adolescents with steatohepatitis.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology Letters - Volume 256, 10 August 2016, Pages 53–63
نویسندگان
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