Demir Mehmet, Cetinavci Dilan, Dogan Kubranur, Elbe Hulya, Saruhan Ercan
Faculty of Medicine, Department of Physiology, Karabuk University, Karabuk, Turkey.
Department of Histology and Embryology, Mugla Training and Research Hospital, Mugla, Turkey.
Arch Physiol Biochem. 2025 Jul 22:1-12. doi: 10.1080/13813455.2025.2535723.
This study explored the neuroprotective effects of honokiol against oxidative stress, neuroinflammation and transforming growth factor-beta1 (TGF-β1) pathways in kainic acid (KA)-induced neurodegeneration in rats. The animals were divided into: control [Honokiol solvent (dimethyl sulphoxide), intraperitoneal for 7 days]; sham [single-dose KA solvent (saline, intracerebroventricular)]; KA (0,5 μg/μl, single-dose, intracerebroventricular); Honokiol [5 mg/kg-intraperitoneal) for 7 days]; and KA+Honokiol [KA single dose and Honokiol (for 7 days)]. Cerebral cortex and hippocampus tissues of the right hemispheres of rat brains were removed and examined biochemically and histopathologically. KA administration caused an increase in malondialdehyde levels and a decrease in reduced glutathione (GSH) and superoxide dismutase (SOD) levels. In addition, interleukin-1β levels and TGF-β1 expression were increased. Honokiol treatment decreased malondialdehyde levels, increased SOD and GSH levels, increased interleukin-1β levels and improved TGF-β1 expression in rats. Our data showed Honokiol has a protective potential against kainic acid-induced neurodegeneration by suppressing oxidative stress, inflammation and TGF-β1 expression.
本研究探讨了厚朴酚对海藻酸（KA）诱导的大鼠神经退行性变中氧化应激、神经炎症和转化生长因子-β1（TGF-β1）信号通路的神经保护作用。将动物分为：对照组[厚朴酚溶剂（二甲基亚砜），腹腔注射7天]；假手术组[单剂量KA溶剂（生理盐水，脑室内注射）]；KA组（0.5μg/μl，单剂量，脑室内注射）；厚朴酚组[5mg/kg腹腔注射，共7天]；KA+厚朴酚组[KA单剂量及厚朴酚（共7天）]。取大鼠右半球的大脑皮质和海马组织进行生化和组织病理学检查。给予KA后，丙二醛水平升高，还原型谷胱甘肽（GSH）和超氧化物歧化酶（SOD）水平降低。此外，白细胞介素-1β水平和TGF-β1表达增加。厚朴酚治疗可降低大鼠丙二醛水平，提高SOD和GSH水平，增加白细胞介素-1β水平并改善TGF-β1表达。我们的数据表明，厚朴酚通过抑制氧化应激、炎症和TGF-β1表达，对海藻酸诱导的神经退行性变具有保护潜力。
