Evaluation of inflammatory miRNA155 and 146a expression in heart tissue of ovalbumin-sensitized male rats

Evaluation of inflammatory miRNA155 and 146a expression in heart tissue of ovalbumin-sensitized male rats


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دانشگاه علوم پزشکی تبریز
دانشگاه علوم پزشکی تبریز

نویسندگان: مهدی حسن پور , رعنا کیهان منش , مهدی احمدی , رضا رهبرقاضی , اکبر دربین

کلمات کلیدی: • Asthma • Cardiovascular injury • Inflammatory miRNAs

نشریه: 56015 , 1 , 9 , 2021

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نویسنده ثبت کننده مقاله مهدی احمدی
مرحله جاری مقاله تایید نهایی
دانشکده/مرکز مربوطه مرکز تحقیقات کاربردی دارویی
کد مقاله 75663
عنوان فارسی مقاله Evaluation of inflammatory miRNA155 and 146a expression in heart tissue of ovalbumin-sensitized male rats
عنوان لاتین مقاله Evaluation of inflammatory miRNA155 and 146a expression in heart tissue of ovalbumin-sensitized male rats
ناشر 5
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 دو – PubMed
آدرس لینک مقاله/ همایش در شبکه اینترنت

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Abstract Introduction: Asthma is a chronic pulmonary inflammation occurred in response to different allergens, leading to respiratory system insufficiency. The production of different inflammatory factors and enhanced immune system response may affect the function of other organs. The aim of this study was to investigate the expression of inflammatory microRNAs in cardiac tissue in asthmatic rat models. Methods: In this study, the animals were allocated into control and asthmatic rats (n=8). To induce asthma, rats were challenged with ovalbumin (OVA). Fourteen days after induction of asthma, rats were euthanized and hematoxylin-eosin (H&E) staining was performed to assess pathological changes in their pulmonary tissue. Serum levels of cardiac enzymes were measured using ELISA kits. Finally, transcription level of inflammatory miRNAs, miRNA-146a and -155, were measured using real-time polymerase chain reaction (PCR) analysis. Results: Based on our findings, histological examination indicated the existence of pathological changes in pulmonary tissue after asthma induction. Bright-field analysis revealed an existence of inflammatory response and cytotoxicity in cardiac tissue. Also, the serum levels of creatine phosphokinase-MB (CpK-MB), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were significantly higher in the serum of asthmatic group compared to control group (P < 0.05). Finally, asthmatic condition induced the expression of (2-fold) miRNA-146a and (1.5-fold)-155 in cardiac tissue, respectively. Conclusion: As a conclusion, it could be concluded that asthmatic condition induces systemic inflammation in cardiac tissue. On a more general note, we propose that therapeutical approaches directed to inflammatory pathway may be required to preserve cardiac injuries caused of asthma.

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نویسنده نفر چندم مقاله
مهدی حسن پوراول
رعنا کیهان منشسوم
مهدی احمدیچهارم
رضا رهبرقاضیپنجم
اکبر دربیندوم

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jrcm-9-11.pdf1400/01/301555960دانلود