Serdaroglu Kasikci Emel, Cevreli Burcu, Sinan Feride Nihal, Gurdere Zeynep, Sonmez Aylin, Sonmez Rumeysa
Uskudar University Faculty of Engineering and Natural Sciences, Department of Molecular Biology and Genetics, Istanbul, Türkiye.
Uskudar University Faculty of Medicine, Department of Physiology, Istanbul, Türkiye.
Medeni Med J. 2025 Mar 28;40(1):18-25. doi: 10.4274/MMJ.galenos.2025.22725.
Aging is a degenerative process. Therefore, the background of our study is to evaluate the effects of boron, one of the important underground resources in Türkiye, on aging and related diseases. This study aimed to assess the antioxidant effect and the cognitive functions of boric acid (BA) in a D-galactose (D-gal)-induced aging model.
Eight male Wistar rats, each 12 weeks old, were split into four groups at random: control, D-gal, BA and D-gal+BA. An experimental aging model was induced by a single subcutaneous injection of D-gal (150 mg/kg/day), and BA (100 mg/kg/day) was administered by oral gavage for 12 weeks. The novel object recognition test (NORT) and Morris water maze (MWM) were used to evaluate the cognitive ability of rats.
At the end of the experimental period, glutathione (GSH) and malondialdehyde (MDA) levels were assessed in serum and brain tissue. The treatment of D-gal induced aging rats with BA significantly decreased the MDA level (p<0.05) and increased the GSH level, although the increase was not significant. Moreover, NORT and MWM tests showed that BA significantly improved (p<0.05) cognitive deficits in D-Gal + BA treated rats.
BA prevents D-gal-induced memory deficit by decreasing oxidative stress. Hence, BA was a good candidate for addressing age-related neurodegenerative disorders and cognitive function improvements.
衰老为一种退行性过程。因此,我们的研究背景是评估硼(土耳其重要的地下资源之一)对衰老及相关疾病的影响。本研究旨在评估硼酸(BA)在D-半乳糖(D-gal)诱导的衰老模型中的抗氧化作用及认知功能。
将8只12周龄雄性Wistar大鼠随机分为四组:对照组、D-gal组、BA组和D-gal+BA组。通过单次皮下注射D-半乳糖(150 mg/kg/天)诱导建立实验性衰老模型,并通过灌胃给予BA(100 mg/kg/天),持续12周。采用新物体识别试验(NORT)和莫里斯水迷宫(MWM)评估大鼠的认知能力。
在实验期末,检测血清和脑组织中的谷胱甘肽(GSH)和丙二醛(MDA)水平。用BA治疗D-gal诱导的衰老大鼠可显著降低MDA水平(p<0.05),并提高GSH水平,尽管升高不显著。此外,NORT和MWM试验表明,BA显著改善(p<0.05)了D-Gal+BA处理大鼠的认知缺陷。
BA通过降低氧化应激预防D-gal诱导的记忆缺陷。因此,BA是解决与年龄相关的神经退行性疾病和改善认知功能的良好候选药物。