中国免疫学杂志2019，Vol.35Issue(2)：146-150,155,6.DOI:10.3969/j.issn.1000-484X.2019.02.004
山奈酚对CUMS抑郁模型大鼠海马神经元过度自噬和氧化应激损伤的保护作用
Protective effects of kaempferol on autophagy-and oxidative stress-mediated injury of hippocampal neuron in CUMS-induced depression model rats
摘要
Abstract
Objective: To investigate the effects and mechanisms of kaempferol on hippocampal neuron in chronic unpredictable mild stress ( CUMS) -induced depression model rats. Methods: 60 rats were divided into control, CUMS, Imipramine ( IMI), Kpf ( 10 mg/kg), Kpf ( 25 mg/kg) and Kpf ( 50 mg/kg) group. Rats were treated with CUMS to establish a depression rat model and rats in Kpf ( 10, 25, 50 mg/kg) were treated with different levels of Kpf respectively and rats in IMI group were treated with IMI ( 10 mg/kg). Rats were sacrificed after rats treating with CUMS for 8 weeks and brain tissues were collected. HE staining was performed for pathological injury and Tunel assay was employed for cell apoptosis. The expressions of Bax, Bcl-2, Casapse-3, Beclin1, P62 and LC3 were measured Western blot. The concentrations of serum SOD, MDA, GSH, NO, IL-1β and TNF-α were determined by kits. Results: Compared with Ctrl group, the injury of hippocampus was aggressive, the apoptosis rate and expression levels of Bax and Caspase-3 were increased significantly, but the expression of Bcl-2 was inhibited; the injury was alleviated, the apoptosis and expressions of Bax and Caspase-3 in IMI and Kpf ( 10, 25, 50 mg/kg) group were inhibited markedly compared with CUMS group, and the expression of Bcl-2 was induced by Kpf. Meanwhile, the level of Beclin1 and the ratio of LC3Ⅱ/LC3Ⅰof CUMS model rats were higher than control rats, and the expression level of P62 was decreased notably. IMI and Kpf ( 10, 25, 50 mg/kg) decreased the protein level of Beclin1 and ratio of LC3Ⅱ/LC3Ⅰin CUMS model rats, and induced the expression of P62. In addition, the concentrations of SOD and GSH of CUMS rats were less than control rats, the concentrations of MDA and inflammatory cytokines NO, IL-1β and TNF-α were increased in CUMS group; IMI and Kpf ( 10, 25, 50 mg/kg) up-regulated the concentrations of SOD and GSH, but down-regulated the concentrations of MDA, NO, IL-1β and TNF-α. Conclusion: Kpf attenuates the hippocampal neuron injury of CUMS model rats by inhibiting autophagy and oxidative stress.关键词
抑郁症/自噬/炎症/氧化应激Key words
Depression/Autophagy/Inflammation/Oxidative stress分类
医药卫生引用本文复制引用
张胜,张尧,李彪,许超,王鹏..山奈酚对CUMS抑郁模型大鼠海马神经元过度自噬和氧化应激损伤的保护作用[J].中国免疫学杂志,2019,35(2):146-150,155,6.基金项目
2014年湖北省自然科学基金项目 (No.2014CFB398) （No.2014CFB398）
