Nazmy Mohamed M, Noor Neveen A, Mohammed Faten F, Khadrawy Yasser A, Radwan Nasr M
Molecular Biology and Biotechnology Department, School of Biotechnology, Badr University, Badr City, Cairo, Egypt.
Zoology Department, Faculty of Science, Cairo University, Giza, Egypt.
Naunyn Schmiedebergs Arch Pharmacol. 2025 Jan 17. doi: 10.1007/s00210-024-03767-4.
Due to the continuous exposure to bisphenol-A (BPA), the current study was conducted to evaluate taurine's neuroprotective action against BPA's adverse effect on the brain. Rats were grouped into control, BPA-treated rats, and taurine + BPA-treated rats. At the end of the 35-day treatment period, the memory of the rats was evaluated using the novel object test and the Y-maze test. An open-field test was used to measure motor activity. The changes in monoamines, monoamine oxidase (MAO), acetylcholinesterase (AChE), Na,K,ATPase, oxidative stress, caspase-3, and histopathology were evaluated in the cortical and hippocampal tissues of all groups. Data analysis by ANOVA revealed that BPA treatment induced motor hyperactivity and short- and long-term memory impairment. In the cortex, BPA decreased serotonin (5-HT), norepinephrine (NE), MAO, Na,K,ATPase, and nitric oxide (NO) and increased dopamine (DA), AChE, lipid peroxidation (MDA), glutathione (GSH), and caspase-3. In the hippocampus, BPA increased 5-HT, DA, NE, MAO, AChE, MDA, NO, GSH, and caspase-3 and decreased Na,K,ATPase. These neurochemical changes were accompanied by significant histopathological alterations. Taurine treatment prevented memory impairment and motor hyperactivity induced by BPA. Taurine attenuated the neurochemical changes, oxidative stress, and caspase-3 level. Taurine improved the histopathological change induced by BPA. In conclusion, taurine significantly prevented BPA-induced cognitive deficits, motor coordination impairments, neurotransmitter imbalances, histopathological alterations, oxidative stress, and apoptosis.
由于持续接触双酚A(BPA),本研究旨在评估牛磺酸对BPA所致脑不良影响的神经保护作用。将大鼠分为对照组、BPA处理组和牛磺酸+BPA处理组。在35天的治疗期结束时,使用新物体试验和Y迷宫试验评估大鼠的记忆力。采用旷场试验测量运动活性。评估了所有组皮质和海马组织中单胺、单胺氧化酶(MAO)、乙酰胆碱酯酶(AChE)、钠钾ATP酶、氧化应激、半胱天冬酶-3和组织病理学的变化。方差分析结果显示,BPA处理导致运动亢进以及短期和长期记忆损伤。在皮质中,BPA降低了血清素(5-HT)、去甲肾上腺素(NE)、MAO、钠钾ATP酶和一氧化氮(NO),并增加了多巴胺(DA)、AChE、脂质过氧化(MDA)、谷胱甘肽(GSH)和半胱天冬酶-3。在海马体中,BPA增加了5-HT、DA、NE、MAO、AChE、MDA、NO、GSH和半胱天冬酶-3,并降低了钠钾ATP酶。这些神经化学变化伴随着明显的组织病理学改变。牛磺酸处理可预防BPA诱导的记忆损伤和运动亢进。牛磺酸减轻了神经化学变化、氧化应激和半胱天冬酶-3水平。牛磺酸改善了BPA诱导的组织病理学变化。总之,牛磺酸显著预防了BPA诱导的认知缺陷、运动协调障碍、神经递质失衡、组织病理学改变、氧化应激和细胞凋亡。