کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5827072 | 1558920 | 2015 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Indomethacin induces endoplasmic reticulum stress, but not apoptosis, in the rat kidney
ترجمه فارسی عنوان
اندومتاسین باعث ایجاد استرس رتیکولوم اندوپلاسمی، اما آپوپتوزیس در کلیه های موش صحرایی
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کلمات کلیدی
PARPATF4ATF6eIF2αNSAIDNrf2HO-1IRE1Cyt CROS - ROSinositol-requiring enzyme 1 - آنزیم مورد نیاز inositol 1ER stress - استرس استEndoplasmic reticulum stress - استرس شبکه آندوپلاسمیIndomethacin - اندومتاسینCHOP - تکه کردنApoptosis - خزان یاختهایcytochrome c - سیتوکروم سیNon-steroidal anti-inflammatory drug - غیر استروئیدی دارو ضد التهابیactivating transcription factor-4 - فعال کردن عامل رونویسی 4activating transcription factor-6 - فعال کردن عامل رونویسی 6Zinc - فلز رویglucose-regulated protein 78 - پروتئین تنظیم شده با گلوکز 78PERK - پرکpoly-ADP ribose polymerase - پلی-ADP ریبوز پلی مرازKidney - کلیهGrp 78 - گروپ 78Reactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب سلولی و مولکولی
چکیده انگلیسی
Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used in clinical practice. However, their use is often associated with adverse effects in the gastrointestinal tract and kidney. Our earlier work with indomethacin, a prototype NSAID, has shown that it induced oxidative stress in the kidney in rats, an event that has been postulated to contribute to pathogenesis of its adverse effects in this organ. Endoplasmic reticulum (ER) stress responses have been shown to occur in response to oxidative stress. We investigated whether this occurred in the rat kidney, in response to indomethacin. For this, Wistar rats were orally gavaged with indomethacin (20Â mg/kg). Markers of ER stress were studied in the kidneys 1, 12 and 24Â h later. GRP78, p-PERK and nuclear sXBP-1, all markers of ER stress, were found to be increased in the rat kidney at 12Â h, in response to indomethacin; levels of these markers fell by 24Â h. The effects seen at 12Â h were attenuated by pre-treatment with zinc, a known anti-oxidant, which has earlier been shown to ameliorate indomethacin-induced oxidative stress. Activation of an ER stress response was not associated with induction of apoptosis, as measured by markers of apoptosis such as release of cytochrome c from mitochondria into the cytosol, activation of caspases 3 and 9, cleavage of poly-ADP ribose polymerase and the presence of DNA laddering. We conclude that indomethacin-induced oxidative stress activated ER stress, but did not lead to apoptosis in the rat kidney.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: European Journal of Pharmacology - Volume 761, 15 August 2015, Pages 199-205
Journal: European Journal of Pharmacology - Volume 761, 15 August 2015, Pages 199-205
نویسندگان
Arumugam Suriyam Nagappan, Joe Varghese, Jithu V. James, Molly Jacob,