Careena S, Sani D, Tan S N, Lim C W, Hassan Shariful, Norhafizah M, Kirby Brian P, Ideris A, Stanslas J, Bin Basri Hamidon, Lim Christopher Thiam Seong
Department of Medicine, Faculty of Medicine and Health Sciences, UPM Serdang 43400, Selangor Darul Ehsan, Malaysia.
Department of Pathology, Faculty of Medicine and Health Sciences, UPM Serdang 43400, Selangor Darul Ehsan, Malaysia.
Evid Based Complement Alternat Med. 2018 Aug 14;2018:9318789. doi: 10.1155/2018/9318789. eCollection 2018.
Cognitive disability is a common feature associated with a variety of neurological conditions including Alzheimer's Disease (AD), Parkinson's Disease (PD), brain injury, and stroke. Emerging evidence has demonstrated that neuroinflammation plays an important role in the development of cognitive impairment. Current available therapies are relatively ineffective in treating or preventing cognitive disabilities, thus representing an important, unfulfilled medical need. Hence, developing potential treatment is one of the major areas of research interest. Edible bird's nests (EBN) are nests formed by swiftlet's saliva containing sialic acid, which is believed to improve brain function. This present study was embarked upon to evaluate the learning and memory enhancing potential effect of EBN by using Morris water maze test in a Wistar rat model of LPS-induced neuroinflammation. LPS elicited cognitive impairment in the rats by significantly increasing the escape latency while decreasing the number of entries in the probe trial, which are coupled with increased production of proinflammatory cytokines (TNF-, IL-1, and IL-6) and oxidative markers (ROS and TBARS) in the hippocampus. Treatment with EBN (125 mg/kg, 250 mg/kg, and 500 mg/kg; p.o.) effectively reversed the effect of LPS on escape latency and probe trial and, in addition, inhibited the LPS-induced upregulation of proinflammatory cytokines and oxidative markers. These findings are suggestive that there is existence of neuroprotective effect contained inside the edible bird's nest.
认知障碍是与多种神经疾病相关的常见特征,这些疾病包括阿尔茨海默病(AD)、帕金森病(PD)、脑损伤和中风。新出现的证据表明,神经炎症在认知障碍的发展中起重要作用。目前可用的治疗方法在治疗或预防认知障碍方面相对无效,因此代表了一个重要的、未得到满足的医疗需求。因此,开发潜在的治疗方法是研究兴趣的主要领域之一。食用燕窝(EBN)是由金丝燕唾液形成的巢穴,其中含有唾液酸,据信唾液酸可改善脑功能。本研究旨在通过在脂多糖(LPS)诱导的神经炎症的Wistar大鼠模型中使用莫里斯水迷宫试验来评估EBN增强学习和记忆的潜在作用。LPS通过显著增加逃避潜伏期,同时减少探测试验中的进入次数,从而引发大鼠的认知障碍,这与海马体中促炎细胞因子(TNF-、IL-1和IL-6)和氧化标志物(ROS和TBARS)的产生增加有关。用EBN(125mg/kg、250mg/kg和500mg/kg;口服)治疗有效地逆转了LPS对逃避潜伏期和探测试验的影响,此外,还抑制了LPS诱导的促炎细胞因子和氧化标志物的上调。这些发现表明食用燕窝中存在神经保护作用。