Metformin Effect on Endocan Biogenesis in Human Endothelial Cells Under Diabetic Condition

Metformin Effect on Endocan Biogenesis in Human Endothelial Cells Under Diabetic Condition


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نویسندگان: المیرا زلالی , آیسا رضابخش , رضا رهبرقاضی , علیرضا گرجانی

کلمات کلیدی: Endocan, Human umbilical vein endothelial cells, High glucose condition, Metformin,Angiogenesis, Functional bioactivity

نشریه: 55048 , 5 , 50 , 2019

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نویسنده ثبت کننده مقاله رضا رهبرقاضی
مرحله جاری مقاله تایید نهایی
دانشکده/مرکز مربوطه مرکز سلولهای بنیادی
کد مقاله 69465
عنوان فارسی مقاله Metformin Effect on Endocan Biogenesis in Human Endothelial Cells Under Diabetic Condition
عنوان لاتین مقاله Metformin Effect on Endocan Biogenesis in Human Endothelial Cells Under Diabetic Condition
ناشر 6
آیا مقاله از طرح تحقیقاتی و یا منتورشیپ استخراج شده است؟ بلی
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 and aim.Endocan is a novel endothelium-derived proteoglycan and mayplay a role in endothelial cells activity under diabetic conditions. Here, we evaluatedthe effect of high glucose concentration (30 mmol glucose) on endocan level in presenceor absence of metformin in human umbilical vein endothelial cells (HUVECs).Methods.Cells were incubated with 30 mmol glucose for 72 h. High glucose content,metformin (2.5 to 500 mmol) and compound C (10 mmol) effects were assessed on cellviability. HUVECs migration was studied by scratch test. The changes in endocan expres-sion and protein level were evaluated by RT-PCR, ELISA and flow cytometry assays. Gri-ess reaction was used to measure NO levels. Functional activity of endothelial cells wasmonitored related to lipoprotein lipase activity using Dil-Ac-LDL uptake. p-AMPK/AMPK ratio was assessed by western blotting.Results.Cells viability significantly was reduced under high glucose condition(p!0.05). 30 mmol glucose inhibited HUVECs migration, whereas these features wereimproved by 50 mmol metformin (p!0.05). Endocan transcription and protein levelswere increased in diabetic HUVECs exposed to metformin (p!0.05). Metforminincreased NO production in HUVECs under high glucose condition (p!0.001). Met-formin increased LDL uptake capacity under high glucose condition (p!0.05). Theaddition of compound C blunted these effects. Western blot analysis confirmed the in-crease of p-AMPK/AMPK ratio in metformin-treated cells.Conclusion.Data demonstrated that metformin could promote angiogenic potential ofendothelial cells which its reduction is a main cause in the development of diabetic footulcer, probably by the regulation of endocan dynamics under high glucose condi-tion.Ó2019 IMSS. Published by Elsevier Inc

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نویسنده نفر چندم مقاله
المیرا زلالیاول
آیسا رضابخشدوم
رضا رهبرقاضیپنجم
علیرضا گرجانیششم

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