کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
8721964 1589452 2018 25 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Fibroblast growth factor 15 deficiency increases susceptibility but does not improve repair to acetaminophen-induced liver injury in mice
ترجمه فارسی عنوان
کمبود فیبروبلاست عامل رشد 15 افزایش حساسیت را افزایش می دهد اما بهبود آسیب کبدی ناشی از استامینوفن در موش ها بهبود نمی یابد
کلمات کلیدی
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی غدد درون ریز، دیابت و متابولیسم
چکیده انگلیسی
The leading cause of acute liver failure (ALF) is hepatotoxicity from acetaminophen (APAP) overdose. However, limited options are available to treat this ALF so stimulating liver regeneration maybe a potential treatment. Our previous study has shown that fibroblast growth factor 15 (FGF15) plays a crucial role in liver regeneration, but the roles of FGF15 in liver injury and repair following APAP-overdose are unknown. In this study, treatment of FGF15 knockout (KO) male mice with APAP at 200, 250, or 300 mg/kg significantly increased the degree of liver injury compared to wild type (WT) mice. To determine the effects of FGF15 deficiency on liver repair following APAP overdose, a similar degree of liver injury was first obtained 24 h after treatment of WT and Fgf15 KO mice with APAP at different dosage. Fgf15 KO mice did not differ from WT mice in liver repair following similar degree of liver injury. In conclusion, we showed that FGF15 deficiency renders mice more susceptible to APAP-induced liver injury but did not seem to affect liver repair or regeneration. This study suggests that in contrast to the critical role that FGF15 plays in promoting liver regeneration following partial hepatectomy, this intestine factor is less involved in liver repair after APAP-induced liver injury.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Digestive and Liver Disease - Volume 50, Issue 2, February 2018, Pages 175-180
نویسندگان
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