医学分子生物学杂志2025，Vol.22Issue(5)：423-429,7.DOI:10.3870/j.issn.1672-8009.2025.05.002
五味子木脂素改善睡眠剥夺模型大鼠神经细胞凋亡和线粒体损伤
Effect of Schisandra chinensis Lignans on Neuronal Apoptosis and Mi-tochondrial Damage in Sleep Deprivation Model Rats
摘要
Abstract
Objective To explore the molecular mechanism by which Schisandra chinensis lig-nans(SCL)improve neuronal apoptosis and mitochondrial damage in the sleep deprivation(SD)model rats.Methods Forty-eight rats were divided into 6 groups:Control group,SD group,modafinil(MOD)group(positive control),and SCL treatment groups at different concentra-tions.The Morris water maze and Y-maze tests were used to assess the escape latency and behavioral accuracy of rats in each group,respectively.HE staining was used to detect hippocampal tissue pathological damage in rats,and TUNEL staining was used to detect cell apoptosis.JC-1 staining and ELISA were used to detect the levels of mitochondrial membrane potential(MMP)and reactive oxygen species(ROS)in rats' brain tissues and cells.An in vitro neuronal damage model was es-tablished using the ROS inducer 2,3-dimethoxy-1,4-naphthoquinone(DMNQ)to stimulate HT-22 cells.CCK-8 was used to measure cell viability.Western blotting was used to detect the expression levels of TLR4,MyD88,and p-NF-κB P65 in cells.Results Compared with those in the Control group,the escape latency of SD rats increased,and behavioral accuracy decreased.In contrast,rats treated with Mod or SCL showed reduced escape latency and increased behavioral accuracy(all P＜0.05).Additionally,compared with rats in the Control group,rats in the SD group exhibited significant hippocampal tissue pathological damage,increased cell apoptosis,decreased MMP lev-els,and increased ROS levels.Mod or SCL intervention improved hippocampal tissue damage and cell apoptosis and reduced neuronal mitochondrial damage in SD rats(all P＜0.05).Cellular exper-imental results showed that HT-22 cells in the DMNQ group had reduced viability,increased apopto-sis,and increased mitochondrial damage and ROS levels when compared with those in the Control group.Mod or SCL treatment significantly improved the DMNQ-induced HT-22 cell damage.Moreover,compared with those in the Control group,the protein expression levels of TLR4,MyD88,and p-NF-κB P65 in the DMNQ group cells were elevated,and Mod or SCL intervention significantly sup-pressed the levels of TLR4,MyD88,and p-NF-κB P65 in DMNQ-treated HT-22 cells.Conclusion SCL improves neuronal apoptosis and mitochondrial damage in SD rats by inhibiting the activation of the TLR4-MyD88-NF-κB pathway.关键词
睡眠剥夺/五味子/木脂素/Toll样受体4/线粒体损伤Key words
sleep deprivation/Schisandra chinensis/lignans/toll-like receptor 4/mitochon-drial damage分类
医药卫生引用本文复制引用
赵艺,李华,胡霞,常海霞..五味子木脂素改善睡眠剥夺模型大鼠神经细胞凋亡和线粒体损伤[J].医学分子生物学杂志,2025,22(5):423-429,7.基金项目
新疆维吾尔自治区自然科学基金(No.2022D01C566) This work was supported by a grant from the Natural Science Foundation of Xinjiang Uygur Autonomous Region(No.2022D01C566) （No.2022D01C566）
