کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2531736 1558944 2014 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction
ترجمه فارسی عنوان
درمان مزمن با متفورمین موجب می شود تا سیگنالینگ گیرنده قرص 4 مانند را دفع کند و اختلالات بطن چپ پس از انفارکتوس قلب را کاهش می دهد
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب سلولی و مولکولی
چکیده انگلیسی

Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100 mg/kg of metformin twice daily for 14 days. Isoproterenol (100 mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LV dp/dtmax and LV dp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50 mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-α and IL-6. However, the lower doses of 25 and 50 mg/kg were more effective than 100 mg/kg. Phosphorylated AMPKα (p-AMPK) in the myocardium was significantly elevated by 25 mg/kg of metformin, slightly by 50 mg/kg, but not by 100 mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: European Journal of Pharmacology - Volume 737, 15 August 2014, Pages 77–84
نویسندگان
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