Samad Noreen, Khalid Arslan, Manzoor Natasha, Abbasi Bakar Bin Khatab, Ejaz Umer, Sumra Ayesha Ahmad, Saleem Tahira, Raish Mohammad, Irfan Ali, Jardan Yousef A Bin
Department of Biochemistry, Faculty of Science, Bahauddin Zakariya University, Multan, 60800, Pakistan.
Department of Chemistry and Chemical Biology, Northeastern University, Boston, MA, 02115, USA.
Sci Rep. 2025 Jul 21;15(1):26410. doi: 10.1038/s41598-025-08014-1.
D-galactose by instigating oxidative stress, inflammation, and degenerative changes, causes neurological problems, i.e., anxiety. Zinc oxide (ZnO)-gallic acid were used to evaluate behavioral, biochemical, neurochemical, and histopathological studies following D-galactose administration in rats. Thirty animals were alienated into five sets (n = 6) i.e., control, D-galactose (300 mg/kg/mL), D-galactose + gallic acid (50 mg/mL/kg), D-galactose + ZnO (10 mg/mL/kg), and D-galactose + ZnO-gallic acid (10 mg/mL/kg). For 28 days, the animals were given their respective treatments intraperitoneally once a day. The anxiety-like behavior was evaluated following the treatment period using behavioral tests, i.e., light-dark and elevated-plus-maze activities. The hippocampus was isolated for biochemical, neurochemical, and histopathological studies. Results showed that ZnO-gallic acid normalize the anxiety-like behavior induced by D-galactose administration. D-galactose induced a reduction in the activity of antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase), increased oxidative-stress markers (malondialdehyde), and elevated inflammatory markers (interleukin-1 and tumor necrosis factor-α). It also impaired serotonergic metabolism and the responsiveness of 5-HT1A receptors, along with causing morphological alterations in the hippocampus. ZnO-gallic acid prevented these effects. These results underscore the protective effects of ZnO-gallic acid NPs against D-galactose-induced negative influences. The present finding suggested that ZnO-gallic acid may be used as a potential agent to treat D-galactose-induced psychiatric illnesses such as anxiety through their antioxidant, anti-inflammatory, and neuromodulatory potential.
D-半乳糖通过引发氧化应激、炎症和退行性变化，导致神经问题，即焦虑。在给大鼠注射D-半乳糖后，使用氧化锌（ZnO）-没食子酸进行行为、生化、神经化学和组织病理学研究。将30只动物分为五组（n = 6），即对照组、D-半乳糖（300 mg/kg/mL）组、D-半乳糖+没食子酸（50 mg/mL/kg）组、D-半乳糖+ZnO（10 mg/mL/kg）组和D-半乳糖+ZnO-没食子酸（10 mg/mL/kg）组。连续28天，每天给动物腹腔注射各自的处理药物。在治疗期结束后，使用行为测试，即明暗箱和高架十字迷宫活动，评估动物的焦虑样行为。分离海马体进行生化、神经化学和组织病理学研究。结果表明，ZnO-没食子酸可使D-半乳糖给药诱导的焦虑样行为恢复正常。D-半乳糖导致抗氧化酶（超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶）活性降低，氧化应激标志物（丙二醛）增加，炎症标志物（白细胞介素-1和肿瘤坏死因子-α）升高。它还损害了血清素能代谢和5-HT1A受体反应性，同时导致海马体形态改变。ZnO-没食子酸可预防这些影响。这些结果强调了ZnO-没食子酸纳米颗粒对D-半乳糖诱导的负面影响的保护作用。目前的研究结果表明，ZnO-没食子酸可能通过其抗氧化、抗炎和神经调节潜力，作为治疗D-半乳糖诱导的精神疾病如焦虑的潜在药物。
