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首页> 外文期刊>Journal of Cellular Physiology >17β‐estradiol rescues damages following traumatic brain injury from molecule to behavior in mice
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17β‐estradiol rescues damages following traumatic brain injury from molecule to behavior in mice

机译：17β雌二醇救助应承担的损害赔偿后的创伤脑损伤从分子到小鼠的行为

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摘要

Traumatic brain injury (TBI) is a public health concern, and causes cognitive dysfunction, emotional disorders, and neurodegeration, as well. The currently available treatments are all symptom‐oriented with unsatifying efficacy. It is highly demanded to understand its underlying mechanisms. Controlled cortical impact (CCI) was used to induce TBI in aged female mice subjected to ovariectomy. Brain damages were assessed with neurological severity score, brain infarction and edema. Morris water maze and elevated plus maze were applied to evaluate the levels of anxiety. Apoptosis in the hippocampus was assayed with Fluoro‐Jade B staining and TUNEL staining. Western blot was employed to measure the expression of NMDA receptor subunits and phosphorylation of ERK1/2, and biochemical assays were used to estimate oxidative stress. 17beta‐Estradiol (E2) was intraperitoneally administered at 10–80?μg/kg once per day for 7 consecutive days before or after CCI. Chronic administration of E2 both before and immediately after CCI conferred neuroprotection, reducing neurological severity score, brain infarction, and edema in TBI mice. Additionally, E2 improved many aspects of deleterious effects of TBI on the hippocampus, including neuronal apoptosis, dysfunction in spatial memory, reduction in NR2B, enhancement of oxidative stress, and activation of ERK1/2 pathway. The present study provides clue for the notion that E2 has therapeutic potential for both prevention and intervention of TBI‐induced brain damages.
机译：创伤性脑损伤(TBI)是一个公共卫生问题,导致认知功能障碍,情感障碍,和neurodegeration好。症状导向与unsatifying功效。对理解其底层高度要求机制。用于诱导在年龄雌性老鼠遭受创伤性脑损伤卵巢切除术。神经严重程度评分、脑梗死和水肿。被应用于评估焦虑的水平。细胞凋亡在海马体化验氟量玉B染色法和TUNEL染色。免疫印迹是用来测量NMDA受体亚基的表达ERK1/2磷酸化,生化分析被用来评估氧化应激。17β雌二醇(E2)腹腔内在10 - 80管理吗?连续几天CCI之前或之后。立即E2之前和管理CCI授予后神经保护,减少神经严重程度评分、脑梗死,和水肿在创伤性脑损伤的老鼠。创伤性脑损伤的许多方面的不良的影响海马体,包括神经元细胞凋亡,在空间记忆障碍,减少NR2B,氧化应激增强,激活ERK1/2通路。线索的概念E2治疗潜在的预防和干预创伤性脑损伤诱导大脑损害。

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