Mashhadizadeh Shahram, Farbood Yaghoub, Dianat Mahin, Khodadadi Ali, Sarkaki Alireza
Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran.
Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran.
Iran J Basic Med Sci. 2017 Apr;20(4):399-407. doi: 10.22038/IJBMS.2017.8581.
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.
TBI was induced by a 200 g weight falling by a 2-m height through a free-falling tube onto the head of anesthetized rat. TBI rats treated immediately after trauma with EA (100 mg/kg, IP) once every 8 hr until 48 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.
TBI induced significant impairments in neurological score, BBB function, PAT and hippocampal LTP in TBI+Veh group in compare with Sham+Veh (<0.001). 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 (<0.001).
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.
诸如学习和记忆障碍等认知缺陷是重度和中度创伤性脑损伤（TBI）后最常见的后遗症。有人提出，天然酚类产物鞣花酸（EA）对脑损伤后的氧化和炎症损伤具有神经保护特性。本研究的目的是探讨EA对大鼠弥漫性TBI后血脑屏障（BBB）破坏、脑组织中肿瘤坏死因子-α（TNF-α）含量升高以及随后出现的神经后遗症、认知和脑电生理缺陷的治疗作用。
通过将200 g重物从2 m高度沿自由落体管落到麻醉大鼠头部来诱导TBI。TBI大鼠在创伤后立即用EA（100 mg/kg，腹腔注射）治疗，每8小时一次，直至48小时后。评估神经学结果、被动回避任务（PAT）、海马长时程增强（LTP）、BBB通透性和脑组织中TNF-α的含量。
与假手术+载体组相比，TBI+载体组中TBI导致神经评分、BBB功能、PAT和海马LTP显著受损（<0.001）。EA治疗显著降低了神经严重程度评分（NSS），恢复了增加BBB通透性、认知和海马LTP异常，并显著降低了TBI导致的脑组织中TNF-α含量升高（<0.001）。
我们的研究结果表明，EA可以恢复NSS、认知和LTP缺陷，并通过恢复BBB通透性以及降低TBI后脑组织中TNF-α的含量来预防脑部炎症。
