Therapeutic effects of ellagic acid on memory, hippocampus electrophysiology deficits, and elevated TNF-α level in brain due to experimental traumatic brain injury
محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 20، شماره: 4
سال انتشار: 1396
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 206
فایل این مقاله در 9 صفحه با فرمت PDF قابل دریافت می باشد
- صدور گواهی نمایه سازی
- من نویسنده این مقاله هستم
استخراج به نرم افزارهای پژوهشی:
شناسه ملی سند علمی:
JR_IJBMS-20-4_008
تاریخ نمایه سازی: 28 مهر 1400
چکیده مقاله:
Objective(s): Cognitive defects such as learning and memory impairment are amongst the most repetitious sequelae after sever and moderate traumatic brain injury (TBI). It was suggested that ellagic acid (EA), an innate phenol product, display neuroprotective properties against oxidative and inflammatory damages after brain injury. The object of the current study was therapeutic properties of EA on blood-brain barrier (BBB) interruption and elevated content of TNF-α in brain tissue followed by neurologic aftereffects, cognitive and brain electrophysiology deficits as outcomes of diffuse TBI in rat. Materials and Methods: TBI was induced by a ۲۰۰ g weight falling by a ۲-m height through a free-falling tube onto the head of anesthetized rat. TBI rats treated immediately after trauma with EA (۱۰۰ mg/kg, IP) once every ۸ hr until ۴۸ hr later. Neurologic outcomes, passive avoidance task (PAT), hippocampal long-term potentiation (LTP), BBB permeability and content of TNF-α in brain tissue were evaluated. Results: TBI induced significant impairments in neurological score, BBB function, PAT and hippocampal LTP in TBI+Veh group in compare with Sham+Veh (P<۰.۰۰۱). EA treatment decreased neurologic severity score (NSS), restored increased BBB permeability, cognitive and hippocampal LTP abnormalities, and elevated brain content of TNF-α due to TBI significantly (P<۰.۰۰۱). Conclusion: Our findings propose that EA can restore NSS, cognitive and LTP deficits and prevent brain inflammation may by restore BBB permeability as well as lowering brain content of TNF-α following TBI.
کلیدواژه ها:
نویسندگان
Shahram Mashhadizadeh
Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran
Yaghoub Farbood
Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran
Mahin Dianat
Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran
Ali Khodadadi
Department of Immunology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran
Alireza Sarkaki
Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran
مراجع و منابع این مقاله:
لیست زیر مراجع و منابع استفاده شده در این مقاله را نمایش می دهد. این مراجع به صورت کاملا ماشینی و بر اساس هوش مصنوعی استخراج شده اند و لذا ممکن است دارای اشکالاتی باشند که به مرور زمان دقت استخراج این محتوا افزایش می یابد. مراجعی که مقالات مربوط به آنها در سیویلیکا نمایه شده و پیدا شده اند، به خود مقاله لینک شده اند :