Wang Gengyin, Wang Liping, Zhang Xiaohan, Wei Zifeng, Wang Kunpeng, Wang Jinhua
School of Basic Medicine, North China University of Science and Technology Tangshan 063210, Hebei, China.
Department of Prevention and Treatment of Infectious Diseases, Fengnan District Center for Disease Control and Prevention Tangshan 063300, Hebei, China.
Int J Clin Exp Pathol. 2024 Dec 15;17(12):469-476. doi: 10.62347/CHBJ5517. eCollection 2024.
Sulforaphane (SFN), an isothiocyanate in cruciferous plants, has been reported to be effective in treating central nervous system diseases. However, how SFN protects the central nervous system needs further study. The aim of this study was to investigate the neuroprotective effect of SFN and its possible mechanism of action.
Sprague-Dawley rats were used to develop a cognitive impairment model. The Morris water maze (MWM) was used to evaluate the effect of SFN on learning and memory, and haematoxylin-eosin (H&E) staining and terminal transferase deoxyuridine nick-end labelling (TUNEL) were used to observe morphologic changes in neurons and neuronal apoptosis in the hippocampus and cortex. An oxidative stress marker kit was used to detect the content and activity of SFN, and the expressions of nuclear factor drythroid-2 related Factor 2 (Nrf2), heme oxygenase 1 (HO-1), and NAD(P)H quinone oxidoreductase 1 (NQO-1) were measured by RT-PCR.
SFN treatment significantly improved cognition, increased the number of neurons, and suppressed neuronal apoptosis. In addition, SFN significantly decreased the content of malondialdehyde (MDA) and enhanced the antioxidant activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the hippocampus and cortex. Furthermore, SFN elevated the expression of Nrf-2, HO-1, and NQO-1.
SFN ameliorated diabetes-induced cognitive dysfunction by activating the Nrf2/HO-1 pathway, providing a new perspective for SFN therapy to delay cognitive impairment in diabetes patients.
萝卜硫素（SFN）是十字花科植物中的一种异硫氰酸盐，据报道其对治疗中枢神经系统疾病有效。然而，SFN如何保护中枢神经系统仍需进一步研究。本研究旨在探讨SFN的神经保护作用及其可能的作用机制。
采用Sprague-Dawley大鼠建立认知障碍模型。利用莫里斯水迷宫（MWM）评估SFN对学习和记忆的影响，采用苏木精-伊红（H&E）染色和末端脱氧核苷酸转移酶介导的缺口末端标记（TUNEL）法观察海马和皮质神经元的形态变化及神经元凋亡情况。使用氧化应激标志物试剂盒检测SFN的含量和活性，并通过RT-PCR检测核因子红细胞2相关因子2（Nrf2）、血红素加氧酶1（HO-1）和NAD（P）H醌氧化还原酶1（NQO-1）的表达。
SFN治疗显著改善认知功能，增加神经元数量，并抑制神经元凋亡。此外，SFN显著降低海马和皮质中丙二醛（MDA）的含量，增强超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）的抗氧化活性。此外，SFN提高了Nrf-2、HO-1和NQO-1的表达。
SFN通过激活Nrf2/HO-1通路改善糖尿病诱导的认知功能障碍，为SFN治疗延缓糖尿病患者认知障碍提供了新的视角。
