بررسی روابط بین میتوکندری، استرس اکسیداتیو و محصولات نهایی گلیکاسیون پیشرفته در بیماری دیابت

نوع مقاله : مروری

نویسندگان

1 استادیار، مرکز تحقیقات گیاهان دارویی، دانشگاه علوم پزشکی جندی شاپور اهواز، اهواز، ایران

2 استادیار، گروه فارماکولوژی، دانشکده داروسازی، دانشگاه علوم پزشکی جندی شاپور اهواز، اهواز، ایران

3 دانشیار، گروه فارماکولوژی، دانشکده داروسازی، دانشگاه علوم پزشکی جندی شاپور اهواز، اهواز، ایران

چکیده

زمینه و هدف: دیابت یک بیماری متابولیک است که می‌تواند نوروپاتی، رتینوپاتی و نفروپاتی ایجاد کند. با توجه به نقش حیاتی میتوکندری در متابولیسم هوازی، عملکرد این ارگانل به‌صورت قابل‌توجهی به پاتوفیزیولوژی دیابت مربوط می­باشد. علاوه بر این، میتوکندری گونه­های فعال اکسیژن را به‌عنوان یک نتیجه از اکسیداسیون سوخت تولید می­کند که شواهد نشان می­دهند این رادیکال­ها و استرس اکسیداتیو ناشی از آن­ها در پاتوفیزیولوژی دیابت و عوارض آن بسیار مهم هستند. محصولات نهایی گلیکاسیون پیشرفته علاوه بر ایجاد استرس اکسیداتیو، عملکرد میتوکندری را نیز مختل می­سازند و می­توان گفت که مسئول عمده عوارض دیابت مانند نفروپاتی، رتینوپاتی می­باشند.
مواد و روش‌ها: این مقاله مروری براساس یافته‌های حاصل از جستجو در پایگاه داده‌های Web of Science، Pubmed و Google Scholar بین سال‌های 1974 تا 2019 تهیه شد.
یافته‌ها: میتوکندری به دلیل نقش اساسی که در تولید انرژی و بقای سلول دارد، مختل شدن عملکرد صحیح آن سلول را به سمت استرس اکسیداتیو و آپوپتوزیس می­کشاند. از طرفی رادیکال­های آزاد و محصولات نهایی گلیکاسیون پیشرفته علاوه بر این که باعث اختلال در عملکرد میتوکندری می‌شود، به‌واسطه خصوصیات عملکردی مشخص خود، در دیابت و پاتوفیزیولوژی دیابت نقش مؤثری دارند.
نتیجه‌گیری: کاهش رادیکال­های آزاد، مهار محصولات نهایی گلیکاسیون پیشرفته و محافظت از عملکرد درست میتوکندری را می‌توان به‌عنوان یک استراتژی برای درمان و بهبود عوارض بیماری دیابت مورد توجه بیشتری قرار داد.

کلیدواژه‌ها

موضوعات


عنوان مقاله [English]

The Relationship Among Mitochondria, Oxidative Stress and Advanced Glycation End Products in Diabetes

نویسندگان [English]

  • Mehdi Goudarzi 1
  • Hamidreza Khalili 2
  • Mohammadreza Rashidi Nooshabadi 2
  • Alireza Malayeri 3
1 Assistant professor, Medicinal Plant Research Center, School of Pharmacy, Ahvaz Jundishapur University of Medical sciences, Ahvaz, Iran
2 Assistant professor, Department of Pharmacology, School of Pharmacy, Ahvaz Jundishapur University of Medical sciences, Ahvaz, Iran
3 Associate professor, Department of Pharmacology, School of Pharmacy, Ahvaz Jundishapur University of Medical sciences, Ahvaz, Iran
چکیده [English]

Introduction: Diabetes is a metabolic disease that can cause neuropathy, retinopathy, and nephropathy. Considering the vital role of mitochondria in aerobic metabolism, its function is significantly related to the pathophysiology of diabetes. In addition, mitochondria produce reactive oxygen species (ROS) from organic fuel molecules during the process of oxidative phosphorylation; according to evidence, ROS and the oxidative stress caused by them are very important for the pathophysiology of diabetes and its complications.In addition to causing oxidative stress, advanced glycation end products (AGEs) impair mitochondrial function and are responsible for major complications of diabetes, such as nephropathy and retinopathy.
Materials and Methods: This review was written based on findings from a search of the Web of Science, PubMed and Google Scholar databases from 1974 to 2019.
Results: Mitochondria, due to their essential role in energy production and cell survival, lead to impaired cell function leading to oxidative stress and apoptosis. On the other hand, free radicals and AGEs due to their specific functional properties result in impairing mitochondrial function and play an important role in the pathophysiology of diabetes.
Conclusion Conclude that the reduction of free radicals, inhibition of AGEs, and protection of the proper function of mitochondria can be considered as the strategy to treat and improve the diabetes complications.

کلیدواژه‌ها [English]

  • Advanced glycation end products
  • diabetes
  • Mitochondria
  • Oxidative stress
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