کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10766554 | 1050655 | 2008 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Protective role of c-Jun N-terminal kinase 2 in acetaminophen-induced liver injury
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Recent studies in mice suggest that stress-activated c-Jun N-terminal protein kinase 2 (JNK2) plays a pathologic role in acetaminophen (APAP)-induced liver injury (AILI), a major cause of acute liver failure (ALF). In contrast, we present evidence that JNK2 can have a protective role against AILI. When male C57BL/6J wild type (WT) and JNK2â/â mice were treated with 300Â mg APAP/kg, 90% of JNK2â/â mice died of ALF compared to 20% of WT mice within 48Â h. The high susceptibility of JNK2â/â mice to AILI appears to be due in part to deficiencies in hepatocyte proliferation and repair. Therefore, our findings are consistent with JNK2 signaling playing a protective role in AILI and further suggest that the use of JNK inhibitors as a potential treatment for AILI, as has been recommended by other investigators, should be reconsidered.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 374, Issue 1, 12 September 2008, Pages 6-10
Journal: Biochemical and Biophysical Research Communications - Volume 374, Issue 1, 12 September 2008, Pages 6-10
نویسندگان
Mohammed Bourdi, Midhun C. Korrapati, Mala Chakraborty, Steven B. Yee, Lance R. Pohl,