کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5505972 | 1400283 | 2017 | 20 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
p16 deficiency promotes nonalcoholic steatohepatitis via regulation of hepatic oxidative stress
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کلمات کلیدی
DMEMDCF-DAMCDHSCsmethionine and choline-deficientDulbecco's modified Eagle's medium - Medal of Eagle اصلاح شده Dulbeccop16 - P16ROS - ROSNon-alcoholic steatohepatitis - استئاتوهپاتیت غیرالکلیOxidative stress - تنش اکسیداتیوHepatic stellate cells - سلولهای ستارهای کبدیNash - نوشPalmitic acid - پالمیتیک اسیدReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Nonalcoholic steatohepatitis (NASH) is characterized by excess accumulation of lipids in liver, accompanied with hepatocyte injury, cell death and inflammation. Although p16 is known as tumor suppressor in multiple cancer types, it remains unclear whether p16 plays a critical role in NASH. To determine whether p16 could play a role in the pathogenesis of NASH, wild-type mice and p16-/- mice were fed on a methionine and choline-deficient (MCD) diet for 3 weeks, and liver steatosis, fibrosis, and inflammation were evaluated. Our data show that p16-/- mice fed with MCD diet displayed more significant hepatic steatosis, hepatocyte damage, increased oxidative stress and inflammatory cell infiltration compared to MCD-fed WT mice. It was also clear that the increased ROS and the accumulation of lipid in BEL-7402Â cells occurred when p16 expression was depleted with siRNA. These findings indicate that p16 may play a critical role in the development of NASH by reining in ROS production and by inhabiting inflammatory response.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 486, Issue 2, 29 April 2017, Pages 264-269
Journal: Biochemical and Biophysical Research Communications - Volume 486, Issue 2, 29 April 2017, Pages 264-269
نویسندگان
Fangqiao Lv, Jun Wu, Dengshun Miao, Wei An, Yutong Wang,