کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6247122 | 1284514 | 2015 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Rapamycin Attenuates Mouse Liver Ischemia and Reperfusion Injury by Inhibiting Endoplasmic Reticulum Stress
ترجمه فارسی عنوان
رامامایسین آسیب شناسی موس کبدی و آسیب مجرای ادراری را با مهار استرس رتیکولوم اندوپلاسمی کاهش می دهد
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موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
عمل جراحی
چکیده انگلیسی
The roles of endoplasmic reticulum (ER) stress in liver ischemia and reperfusion injury (IRI) have been well recognized. However, the impact of rapamycin (Rapa), a broadly used immunosuppressive agent in human liver transplantation, on ER stress during IRI remains unclear. This study was designed to investigate the roles of Rapa in the regulation of ER stress in vivo and in vitro. In a mouse liver partial warm ischemia and reperfusion mode, we demonstrated that Rapa markedly protected livers from IRI, as evidenced by serum alanine aminotransferase (sALT) levels and liver histology. Then we also confirmed the protection of Rapa from thapsigargin (Tg)-induced cell death in primary hepatocytes. Both in vivo and in vitro experiments showed that the ER stress markers were markedly up-regulated by IRI and Tg treatment, whereas they were down-regulated by Rapa pretreatment, as monitored by Western blot at the protein levels and by quantitative reverse transcription polymerase chain reaction (RT-PCR) at the messenger RNA (mRNA) levels. In addition, it was also revealed that Rapa was able to remarkably inhibit the mammalian target of rapamycin (mTOR) pathway and enhance autophagy both in IR-stressed livers and Tg-treated primary hepatocytes. Thus, these results suggest that Rapa protects livers from IRI through inhibiting the ER stress pathway.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Transplantation Proceedings - Volume 47, Issue 6, JulyâAugust 2015, Pages 1646-1652
Journal: Transplantation Proceedings - Volume 47, Issue 6, JulyâAugust 2015, Pages 1646-1652
نویسندگان
J. Zhu, X. Hua, D. Li, J. Zhang, Q. Xia,