کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3840821 | 1247940 | 2010 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Neutrophil elastase contributes to the development of ischemia/reperfusion-induced liver injury by decreasing the production of insulin-like growth factor-I in rats
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کلمات کلیدی
IGF-IEMAP-IIPGI2CGRPCOXALTNOSiNOSMPO - DFOI/R - I / Rinducible NOS - NOS قابل القاییAST - آسپارتات ترانس آمینازAspartate aminotransferase - آسپارتات ترانس آمیناز یا AST Alanine aminotransferase - آلانین آمینوترانسفرازcyclooxygenase - آنزیم سیکلواکسیژنازneutrophil elastase - الاستاز نوتروفیلIndomethacin - اندومتاسینischemia/reperfusion - ایسکمی / رپرفیوژنTUNEL - تونلmyeloperoxidase - میلوپراکسیداز nitric oxide synthase - نیتریک اکسید سنتازprostacyclin - پروستاسیکلینcalcitonin gene-related peptide - پپتید مرتبط با ژن کلسی تونین
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
پزشکی و دندانپزشکی (عمومی)
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چکیده انگلیسی
Neutrophil elastase (NE) decreases the endothelial production of prostacyclin (PGI2) through the inhibition of endothelial nitric oxide synthase (NOS) activation and thereby contributes to the development of ischemia/reperfusion (I/R)-induced liver injury. We previously demonstrated that calcitonin gene-related peptide (CGRP) released from sensory neurons increases the insulin-like growth factor- I (IGF-I) production and thereby reduces I/R-induced liver injury. Because PGI2 is capable of stimulating sensory neurons, we hypothesized that NE contributes to the development of I/R-induced liver injury by decreasing IGF-I production. In the present study, we examined this hypothesis in rats subjected to hepatic I/R. Ischemia/reperfusion-induced decreases of hepatic tissue levels of CGRP and IGF-I were prevented significantly by NE inhibitors, sivelestat, and L-658, 758, and these effects of NE inhibitors were reversed completely by the nonselective cyclooxygenase inhibitor indomethacin (IM) and the nonselective NOS inhibitor L-NAME but not by the selective inducible NOS inhibitor 1400W. I/R-induced increases of hepatic tissue levels of caspase-3, myeloperoxidase and the number of apoptotic cells were inhibited by NE inhibitors, and these effects of NE inhibitors were reversed by IM and L-NAME but not by 1400W. Administration of iloprost, a stable PGI2 analog, produced effects similar to those induced by NE inhibitors. Taken together, these observations strongly suggest that NE may play a critical role in the development of I/R-induced liver injury by decreasing the IGF-I production through the inhibition of sensory neuron stimulation, which may lead to an increase of neutrophil accumulation and hepatic apoptosis through activation of caspase-3 in rats.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Translational Research - Volume 155, Issue 6, June 2010, Pages 294-304
Journal: Translational Research - Volume 155, Issue 6, June 2010, Pages 294-304
نویسندگان
Miho Kawai, Naoaki Harada, Hiromitsu Takeyama, Kenji Okajima,