کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8267464 | 1534944 | 2016 | 35 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The antioxidant transcription factor Nrf2 contributes to the protective effect of mild thermotolerance (40 °C) against heat shock-induced apoptosis
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کلمات کلیدی
GCLKelch ECH associating protein 1human cervical carcinoma cellsD-MEMMOPSGPx1Heme oxygenase-1HSF1GSRATF-3MnSODHspNOSDAFHRPHO-1GSTFITCGSHG6PDDTTEGTABSA - BSAkeap1 - buy1l-NAME - L-NAMEl-NG-Nitroarginine methyl ester - L-NG-Nitroarginine متیل استرMdm2 - MDM2bovine serum albumin - آلبومین سرم گاوEDTA - اتیلن دی آمین تترا استیک اسید ethylene diamine tetraacetic acid - اتیلن دیامین تتراستیک اسیدethylene glycol tetraacetic acid - اتیلن گلیکول تتراستیک اسیدDulbecco's modification of Eagle's medium - اصلاح Dulbecco از محیط عقابdihydroethidium - دی هیدروتیدیمdiaminofluorescein - دیامین فلوئورسینdithiothreitol - دیتیوتریتولmanganese superoxide dismutase - سوپر اکسید دیسموتاز منگنزendoplasmic reticulum - شبکه آندوپلاسمی heat shock factor 1 - عامل شوک گرما 1antioxidant response element - عنصر پاسخ آنتی اکسیدانActivating transcription factor-3 - فعال کردن عامل رونویسی 3fluorescein isothiocyanate - فلوئورسین ایسوتیوسیاناتglutamate cysteine ligase - لیگاز سیتئین گلوتاماتMouse double minute 2 - ماوس دو دقیقه 2nitric oxide synthase - نیتریک اکسید سنتازARE - هستندDHE - وHorseradish peroxidase - پراکسیداز هوررادیشHeat shock protein - پروتئین شوک حرارتHela - کاملreduced glutathione - کاهش گلوتاتیونglutathione S-transferase - گلوتاتیون S-ترانسفرازglutathione peroxidase 1 - گلوتاتیون پراکسیداز 1
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The exposure of cells to low doses of stress induces adaptive survival responses that protect cells against subsequent exposure to toxic stress. The ability of cells to resist subsequent toxic stress following exposure to low dose heat stress at 40 °C is known as mild thermotolerance. Mild thermotolerance involves increased expression of heat shock proteins and antioxidants, but the initiating factors in this response are not understood. This study aims to understand the role of the Nrf2 antioxidant pathway in acquisition of mild thermotolerance at 40 °C, and secondly, whether the Nrf2 pathway could be involved in the protective effect of thermotolerance against heat-shock (42 °C)-induced apoptosis. During cell preconditioning at 40 °C, protein expression of the Nrf2 transcription factor increased after 15-60 min. In addition, levels of the Nrf2 targets MnSOD, catalase, heme oxygenase-1, glutamate cysteine ligase and Hsp70 increased at 40 °C. Levels of these Nrf2 targets were enhanced by Nrf2 activator oltipraz and decreased by shRNA targeting Nrf2. Levels of pro-oxidants increased after 30-60 min at 40 °C. Pro-oxidant levels were decreased by oltipraz and increased by knockdown of Nrf2. Increased Nrf2 expression and catalase activity at 40 °C were inhibited by the antioxidant PEG-catalase and by p53 inhibitor pifithrin-α. These results suggest that mild thermotolerance (40 °C) increases cellular pro-oxidant levels, which in turn activate Nrf2 and its target genes. Moreover, Nrf2 contributes to the protective effect of thermotolerance against heat-shock (42 °C)-induced apoptosis, because Nrf2 activation by oltipraz enhanced thermotolerance, whereas Nrf2 knockdown partly reversed thermotolerance. Improved knowledge about the different protective mechanisms that mild thermotolerance can activate is crucial for the potential use of this adaptive survival response to treat stress-related diseases.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 99, October 2016, Pages 485-497
Journal: Free Radical Biology and Medicine - Volume 99, October 2016, Pages 485-497
نویسندگان
Audrey Glory, Diana A. Averill-Bates,