Nervous System Stem Cell Research Center, Semnan University of Medical Sciences, Semnan, Iran.
Department of Anatomical Sciences, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran.
Metab Brain Dis. 2023 Dec;38(8):2691-2720. doi: 10.1007/s11011-023-01257-9. Epub 2023 Oct 16.
Bisphenol A (BPA) is an endocrine-disrupting chemical commonly utilized in the manufacture of plastics, which may cause damage to brain tissue. Curcumin is a phytochemical with protective effects against neurological and mental diseases. The purpose of this research was to evaluate whether nanomicellar curcumin (NmCur) might protect rats against BPA-induced learning and memory deficits. After determining the proper dose of BPA, the animals were randomly divided into 8 groups (8 rats in each group) receiving dextrose 5% (as vehicle of NmCur) (Dex), sesame oil (as vehicle of BPA) (Sea), Sea plus Dex, NmCur (50 mg/kg), BPA (50 mg/kg), and 50 mg/kg BPA plus 10, 25, and 50 mg/kg NmCur groups, respectively. Behavioral tests performed using passive avoidance training (PAT), open-field (OF), and Morris water maze (MWM) tests. The expression of oxidative stress markers, proinflammatory cytokines, oxidative stress-scavenging enzymes, glutamate receptors, and MAPK and memory-related proteins was measured in rat hippocampus and cortical tissues. BPA up-regulated ROS, MDA, TNF-α, IL-6, IL-1β, SOD, GST, p-P38, and p-JNK levels; however, it down-regulated GSH, GPx, GR, CAT, p-AKT, p-ERK1/2, p-NR1, p-NR2A, p-NR2B, p-GluA1, p-CREB, and BDNF levels. BPA decreased step-through latency (STL) and peripheral and total, but not central, locomotor activity. It increased the time to find the hidden platform, the mean of escape latency time, and the traveled distance in the target quadrant, but decreased the time spent in the target quadrant. The combination of BPA (50 mg/kg) and NmCur (25 and 50 mg/kg) reversed all of BPA's adverse effects. Therefore, NmCur exhibited neuroprotective effects against subacute BPA-caused learning and memory impairment.
双酚 A(BPA)是一种常用于制造塑料的内分泌干扰化学物质,可能会对脑组织造成损害。姜黄素是一种具有神经和精神疾病保护作用的植物化学物质。本研究旨在评估纳米胶束姜黄素(NmCur)是否可能保护大鼠免受 BPA 引起的学习和记忆缺陷。在确定 BPA 的适当剂量后,动物被随机分为 8 组(每组 8 只),分别接受 5%葡萄糖(作为 NmCur 的载体)(Dex)、芝麻油(作为 BPA 的载体)(Sea)、Sea 加 Dex、NmCur(50mg/kg)、BPA(50mg/kg)和 50mg/kg BPA 加 10、25 和 50mg/kg NmCur 组。使用被动回避训练(PAT)、旷场(OF)和 Morris 水迷宫(MWM)测试进行行为测试。测量大鼠海马和皮质组织中氧化应激标志物、促炎细胞因子、氧化应激清除酶、谷氨酸受体以及 MAPK 和记忆相关蛋白的表达。BPA 上调 ROS、MDA、TNF-α、IL-6、IL-1β、SOD、GST、p-P38 和 p-JNK 水平;然而,它下调了 GSH、GPx、GR、CAT、p-AKT、p-ERK1/2、p-NR1、p-NR2A、p-NR2B、p-GluA1、p-CREB 和 BDNF 水平。BPA 降低了步出潜伏期(STL)和外周和总,但不是中央,运动活性。它增加了找到隐藏平台的时间、逃避潜伏期时间的平均值、目标象限的行驶距离,但减少了目标象限的时间。BPA(50mg/kg)与 NmCur(25 和 50mg/kg)的组合逆转了 BPA 的所有不良反应。因此,NmCur 对亚急性 BPA 引起的学习和记忆损伤表现出神经保护作用。