Quercetin alleviates high glucose-induced damage on human umbilical vein endothelial cells by promoting autophagy

Quercetin alleviates high glucose-induced damage on human umbilical vein endothelial cells by promoting autophagy


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نویسندگان: آیسا رضابخش , رضا رهبرقاضی , فرزانه فتحی , آزاده منتصری , علیرضا گرجانی

کلمات کلیدی: Human umbilical vein endothelial cells; Quercetin;Diabetic condition; Autophagy status

نشریه: 27532 , 1 , 56 , 2018

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نویسنده ثبت کننده مقاله رضا رهبرقاضی
مرحله جاری مقاله تایید نهایی
دانشکده/مرکز مربوطه مرکز سلولهای بنیادی
کد مقاله 65052
عنوان فارسی مقاله Quercetin alleviates high glucose-induced damage on human umbilical vein endothelial cells by promoting autophagy
عنوان لاتین مقاله Quercetin alleviates high glucose-induced damage on human umbilical vein endothelial cells by promoting autophagy
ناشر 6
آیا مقاله از طرح تحقیقاتی و یا منتورشیپ استخراج شده است؟ خیر
عنوان نشریه (خارج از لیست فوق)
نوع مقاله Original Article
نحوه ایندکس شدن مقاله ایندکس شده سطح یک – ISI - Web of Science
آدرس لینک مقاله/ همایش در شبکه اینترنت

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Background: Quercetin, a flavonoid antioxidant, has been found to exert therapeutic effects in diabetic condition. Autophagy represents a homeostatic cellular mechanism for the turnover of unfolds proteins and damaged organelles through a lysosome-dependent degradation manner. We speculated that quercetin could protect endothelial cells against high glucose-induced damage by promoting autophagic responses. Methods: HUVECs viability was evaluated by MTT method. Griess and TBARS assays were used to monitor the levels of NO and MDA, respectively. Intracellular ROS generation was determined in DCFDA-stained cells analyzed by flow cytometry. To investigate the role of quercetin in endothelial cell migratory behavior, we used a scratch test. The level of autophagy proteins LC3, Beclin-1 and P62 were measured by western blotting technique. Results: Our results showed that quercetin had the potential to increase cell survival after exposure to high glucose (P<0.05). Total levels of oxidative stress markers were profoundly decreased and the activity of GSH was increased by quercetin (P<0.05). High glucose suppressed HUVECs migration to the scratched area (P<0.05). However, a significant stimulation in cell migration was observed after exposure to quercetin (P<0.05). Based on data, autophagy was blocked at the late stage by high glucose concentration while quercetin enhanced autophagic response by reducing the P62 level coincided with the induction of Beclin-1 and LC3-II to LC3-I ratio (P<0.05). All these beneficial effects were reversed by 3-methyladenine as an autophagy inhibitor. Conclusion: Together, our data suggest that quercetin could protect HUVECs from high glucose induced-damage possibly by activation of the autophagy response.

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نویسنده نفر چندم مقاله
آیسا رضابخشاول
رضا رهبرقاضیدوم
فرزانه فتحیچهارم
آزاده منتصریپنجم
علیرضا گرجانیششم

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نام فایل تاریخ درج فایل اندازه فایل دانلود
Aysa10.1016@j.phymed.2018.11.008.pdf1397/08/265595314دانلود