این سایت در حال حاضر پشتیبانی نمی شود و امکان دارد داده های نشریات بروز نباشند
صفحه اصلی
درباره پایگاه
فهرست سامانه ها
الزامات سامانه ها
فهرست سازمانی
تماس با ما
JCR 2016
جستجوی مقالات
سه شنبه 28 بهمن 1404
Iranian Journal of Basic Medical Sciences
، جلد ۱۸، شماره ۹، صفحات ۸۶۷-۸۷۲
عنوان فارسی
چکیده فارسی مقاله
کلیدواژههای فارسی مقاله
عنوان انگلیسی
Melatonin treatment reduces astrogliosis and apoptosis in rats with traumatic brain injury
چکیده انگلیسی مقاله
Objective(s):Melatonin is known as an anti-inflammatory agent, and it has been proven to exert neuroprotection through inhibition of cell death (apoptosis) in several models of brain injury.Secondary injury following the primary traumatic brain injury (TBI) results in glial cells activation, especially astrocytes. In fact, astrocyte activation causes the production of pro-inflammatory cytokines that may lead to secondary injury. Since most TBI research studies have focused on injured neurons and paid little attention to glial cells, the aim of current study was to investigate the effects of melatonin against astrocytes activation (astrogliosis), as well as inhibition of apoptosis in brain tissue of male rats after TBI. Materials and Methods: The animals were randomly allocated into five groups: sham group, TBI+ vehicle group (1% ethanol in saline) and TBI+ melatonin groups (5 mg/kg, 10 mg/kg and 20 mg/kg). All rats were intubated and then exposed to diffuse TBI, except for the sham group. Immunohistochemical methods were conducted using glial fibrillary acidic protein (GFAP) marker and TUNEL assay to evaluate astrocyte reactivity and cell death, respectively. Results: The results showed that based on the number of GFAP positive astrocytes in brain cortex, astrogliosis was reduced significantly (P< 0.05) in melatonin- treated groups (no dose dependent) compared to the vehicle group. Furthermore, based on TUNEL results, melatonin treatment considerably reduced the number of apoptotic cells (P< 0.05). Conclusion:In total, the present findings suggest that melatonin treatment following TBI diminishes astrocyte reactivity and neuronal cells apoptosis in brain cortex in the rat model.
کلیدواژههای انگلیسی مقاله
نویسندگان مقاله
عبدالرضا بابایی | abdolreza babaee
department of anatomical sciences, afzalipour school of medicine, kerman university of medical sciences, kerman, iran
سازمان اصلی تایید شده
: دانشگاه علوم پزشکی کرمان (Kerman university of medical sciences)
سید حسن افتخار واقفی | seyed hassan eftekhar vaghefi
department of anatomical sciences, afzalipour school of medicine, kerman university of medical sciences, kerman, iran
سازمان اصلی تایید شده
: دانشگاه علوم پزشکی کرمان (Kerman university of medical sciences)
مجید اسدی شکاری | majid asadi shekaari
neuroscience research center, institute of neuropharmacology, kerman university of medical sciences, kerman, iran
سازمان اصلی تایید شده
: دانشگاه علوم پزشکی کرمان (Kerman university of medical sciences)
نادر شاهرخی | nader shahrokhi
department of physiology, afzalipour school of medicine, kerman university of medical sciences, kerman, iran
سازمان اصلی تایید شده
: دانشگاه علوم پزشکی کرمان (Kerman university of medical sciences)
سامره دهقانی سلطانی | samereh dehghani soltani
department of anatomical sciences, afzalipour school of medicine, kerman university of medical sciences, kerman, iran
سازمان اصلی تایید شده
: دانشگاه علوم پزشکی کرمان (Kerman university of medical sciences)
رضا ملک پور افشار | reza malekpour afshar
department of pathology, afzalipour school of medicine, kerman university of medical sciences, kerman, iran
سازمان اصلی تایید شده
: دانشگاه علوم پزشکی کرمان (Kerman university of medical sciences)
محسن بصیری | mohsen basiri
neuroscience research center, institute of neuropharmacology, kerman university of medical sciences, kerman, iran
سازمان اصلی تایید شده
: دانشگاه علوم پزشکی کرمان (Kerman university of medical sciences)
نشانی اینترنتی
http://ijbms.mums.ac.ir/article_5207.html
فایل مقاله
فایلی برای مقاله ذخیره نشده است
کد مقاله (doi)
زبان مقاله منتشر شده
en
موضوعات مقاله منتشر شده
نوع مقاله منتشر شده
Original Article
برگشت به:
صفحه اول پایگاه
|
نسخه مرتبط
|
نشریه مرتبط
|
فهرست نشریات