این سایت در حال حاضر پشتیبانی نمی شود و امکان دارد داده های نشریات بروز نباشند
Basic and Clinical Neuroscience، جلد ۱۱، شماره ۶، صفحات ۷۹۵-۸۰۴
عنوان فارسی
چکیده فارسی مقاله
کلیدواژه‌های فارسی مقاله
عنوان انگلیسی Dalteparin as a Novel Therapeutic Agent to Prevent Diabetic Encephalopathy by Targeting Oxidative Stress and Inflammation
چکیده انگلیسی مقاله Introduction: Hepcidin is the main modulator of systemic iron metabolism, and its role in the brain has been clarified recently. Studies have shown that hepcidin plays an important role in neuronal iron load and inflammation. This issue is of significance because neuronal iron load and inflammation are pathophysiological processes that are highly linked to neurodegeneration. Moreover, the activity of hepcidin has recently been manipulated to recover the neuronal impairment caused by brain inflammation in animal models. Methods: Streptozotocin (STZ) was used to induce type 1 diabetes. Male Wistar rats (n = 40) with a weight range of 200–250 g were divided into control, diabetic, diabetic + insulin, and diabetic + dalteparin groups. Dalteparin (100 mg/kg IP) and insulin (100 mg/kg SC) were administered for 8 weeks. At the end of the experiment, Y-maze and passive avoidance tasks were carried out. The animals were perfused randomly and their hippocampal tissue was isolated for the analysis of markers such as lipid peroxidation like Malondialdehyde (MDA), hepcidin expression, iron, and ferritin. Blood samples were taken for the measurement of serum inflammatory cytokine Interleukin (IL)-6. Results: The findings indicated that treatment with dalteparin reduced IL-6, MDA, ferritin, and hepcidin expression in diabetic rats compared to treatment with insulin (P< 0.05). Moreover, treatment with dalteparin did not decrease the iron level or prevented its decline. Conclusion: Treatment with dalteparin improved the cognitive dysfunctions and symptoms of Alzheimer disease in STZ-induced diabetic rats by appropriately modulating and reducing oxidative stress and neuroinflammation. This may enhance the existing knowledge of therapeutics to reduce cognitive impairment in diabetes and is suggested to be a potential therapeutic agent in diabetes.
کلیدواژه‌های انگلیسی مقاله Type1 diabetes, Diabetic encephalopathy, Hepcidin, Iron
نویسندگان مقاله | Motahareh Zeinivand
Department of Physiology, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran.


| Arezo Nahavandi
Department of Physiology, School of Medicine, Iran University of Medical Sciences, Iran, Iran.


| Tourandokht Baluchnejadmojarad
Department of Physiology, School of Medicine, Iran University of Medical Sciences, Iran, Iran.


| Mehrdad Roghani
Department of Physiology, School of Medicine, Shahed University, Tehran, Iran.


| Fereshteh Golab
Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran.
نشانی اینترنتی http://bcn.iums.ac.ir/browse.php?a_code=A-10-1775-1&slc_lang=en&sid=1
فایل مقاله فایلی برای مقاله ذخیره نشده است
کد مقاله (doi)
زبان مقاله منتشر شده en
موضوعات مقاله منتشر شده Cellular and molecular Neuroscience
نوع مقاله منتشر شده Original
برگشت به: صفحه اول پایگاه   |   نسخه مرتبط   |   نشریه مرتبط   |   فهرست نشریات