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The Effects of Incensole Acetate on Neuro-inflammation, Brain-Derived Neurotrophic Factor and Memory Impairment Induced by Lipopolysaccharide in Rats
Neurochemical Research ( IF 3.7 ) Pub Date : 2021-06-26 , DOI: 10.1007/s11064-021-03381-3
Narges Marefati 1 , Farimah Beheshti 2, 3 , Farzaneh Vafaee 4 , Moslem Barabadi 5 , Mahmoud Hosseini 6, 7
Affiliation  

Incensole acetate (IA) is a major component of Boswellia serrata resin that has been shown to have anti-inflammatory, anti-oxidant and neuroprotective properties. The present study determined the effect of IA on lipopolysaccharide (LPS)-induced memory impairment, and hippocampal cytokines and oxidative stress indicators level. We used 32 Wistar rats (220–250 g weight) randomly divided into four groups. The control group, which only received the saline-diluted DMSO (vehicle); LPS group which received LPS and was treated with the vehicle; and two IA-treated groups which received 2.5 or 5 mg/ kg IA before LPS injection. Morris water maze (MWM) and passive avoidance (PA) tests were performed. Finally, the brains were removed and were used to assess cytokines levels and oxidative stress status. Compared to the LPS group, IA administration reduced the time spent and path traveled to reach the hidden platform during 5 days of learning in MWM while increased the time spent in the target quadrant in the probe test. Moreover, IA increased latency while decreased entry number and time spent in the dark chamber of PA test compared to the LPS group. Additionally, pre-treatment with IA attenuated interleukin(IL)-6, tumor necrosis alpha (TNF-α), glial fibrillary acidic protein (GFAP), malondialdehyde (MDA) and nitric oxide (NO) metabolites levels while increased those of IL-10, total thiol, superoxide dismutase (SOD), catalase (CAT) and brain-derived neurotrophic factor (BDNF). Our results indicated that IA improved LPS-induced learning and memory impairments. The observed effects seem to be mediated via a protective activity against neuro-inflammation and brain tissue oxidative damage and through improving BDNF.



中文翻译:


香薰醋酸酯对脂多糖所致大鼠神经炎症、脑源性神经营养因子及记忆障碍的影响



醋酸熏香 (IA) 是齿叶乳香树脂的主要成分,已被证明具有抗炎、抗氧化和神经保护特性。本研究确定了IA对脂多糖(LPS)引起的记忆障碍以及海马细胞因子和氧化应激指标水平的影响。我们使用 32 只 Wistar 大鼠(体重 220-250 克),随机分为四组。对照组,仅接受生理盐水稀释的DMSO(媒介物); LPS组接受LPS并用媒介物治疗;以及两个 IA 治疗组,在注射 LPS 之前接受 2.5 或 5 mg/kg IA。进行莫里斯水迷宫(MWM)和被动回避(PA)测试。最后,取出大脑并用于评估细胞因子水平和氧化应激状态。与LPS组相比,IA给药减少了MWM学习5天期间到达隐藏平台所花费的时间和路径,同时增加了探测测试中在目标象限所花费的时间。此外,与 LPS 组相比,IA 增加了潜伏期,同时减少了 PA 测试暗室的进入次数和时间。此外,IA 预处理可减弱白细胞介素 (IL)-6、肿瘤坏死 α (TNF-α)、神经胶质纤维酸性蛋白 (GFAP)、丙二醛 (MDA) 和一氧化氮 (NO) 代谢物水平,同时增加 IL-6 代谢物水平10、总硫醇、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和脑源性神经营养因子(BDNF)。我们的结果表明,IA 改善了 LPS 引起的学习和记忆障碍。观察到的效果似乎是通过针对神经炎症和脑组织氧化损伤的保护活性以及通过改善 BDNF 来介导的。

更新日期:2021-07-24
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