文章摘要
潘翰逸 ,陈志颖 ,张曼青.深部脑磁刺激改善大鼠卒中后抑郁样行为[J].神经损伤功能重建,2024,(1):8-11
深部脑磁刺激改善大鼠卒中后抑郁样行为
Deep Brain Magnetic Stimulation Improves Depression-like Behavior after Stroke in Rats PAN
  
DOI:
中文关键词: 卒中后抑郁  深部脑磁刺激  小胶质细胞  炎性因子  前额叶
英文关键词: post-stroke depression  deep brain magnetic stimulation  microglia  inflammatory factors  prefrontal lobe
基金项目:江西省自然科学基 金(常压高浓度氧 调控BNIP3介导的 线粒体自噬改善慢 性脑缺血脑损害的 机制研究,No. 202 24BAB216045)
作者单位
潘翰逸1 ,陈志颖2 ,张曼青3 1. 九江学院化学化 工学院 2. 九江学院附属医 院 3. 九江学院基础医 学院 
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中文摘要:
      目的:探讨深部脑磁刺激(DMS)对卒中后抑郁(PSD)模型大鼠抑郁样行为的治疗作用及其可能机 制。方法:糖水偏好实验和旷场实验筛选42只正常的雄性成年SD大鼠,随机分为假手术组(Sham组,n= 6)、卒中组(Stroke组,n=12)、卒中后抑郁组(PSD组,n=12)、深部脑磁刺激治疗组[(PSD+DMS)组,n=12];后 3组颈总动脉线栓再灌注法构建脑缺血模型;假手术组只分离颈总动脉不结扎;PSD组和(PSD+DMS)组接 受3周慢性温和应激制备PSD模型;(PSD+DMS)组每天接受40 min的40 Hz深部脑磁刺激治疗,共2周。 旷场实验检测各组大鼠运动功能和焦虑样行为;糖水偏好实验检测各组大鼠快感缺失抑郁样行为;免疫荧 光染色检测各组大鼠前额叶小胶质细胞激活标志物Iba-1的表达水平;蛋白质免疫印迹技术检测各组大鼠 前额叶小胶质细胞激活阳性蛋白CD11b及炎性因子IL-1β和TNF-α的表达。结果:(PSD+DMS)组大鼠抑郁 样行为较PSD组明显好转。卒中组大鼠前额叶小胶质细胞激活增加,炎性因子IL-1β和TNF-α的蛋白表达 升高,PSD 组大鼠前额叶小胶质细胞激活进一步增加,炎性因子 IL-1β和 TNF-α的蛋白表达进一步升高。 (PSD+DMS)组大鼠前额叶小胶质细胞激活减少,炎性因子IL-1β和TNF-α的蛋白表达降低。结论:DMS治 疗可有效地改善PSD大鼠的抑郁样行为。抑制前额叶皮质小胶质细胞激活和炎性因子的表达可能是其潜 在的抗抑郁作用机制。
英文摘要:
      To investigate therapeutic effects of deep brain magnetic stimulation (DMS) on depressive-like behavior in a post-stroke depression (PSD) rat model and its potential mechanisms. Methods: Total 42 adult male SD rats were screened using sucrose preference test and open field test. They were randomly divided into sham surgery group (Sham group, n=6), stroke group (Stroke group, n=12), PSD group (n=12) , and (PSD + DMS) group (n=12). Cerebral ischemia models were established induced by bilateral common carotid artery occlusion and reperfusion in groups stroke, PSD and (PSD+DMS). The common carotid artery of sham group was only separated without ligation. Groups PSD and (PSD + DMS) accepted chronic mild stress for 3 weeks, while (PSD+DMS) group rats accepted 40 Hz deep brain magnetic stimulation for 40 minutes per day for 2 weeks. The open field test was used to evaluate locomotor activity and anxiety-like behavior, while the sucrose preference test assessed anhedonia-like behavior. Immunofluorescence staining was performed to measure the expression level of Iba-1, a marker of glial cell activation, in the frontal lobe. Protein immunoblotting technique was used to detect the expression of CD11b, a marker of glial cell activation, as well as inflammatory cytokines IL-1 β and TNF-α in the frontal lobe. Results: Treatment with DMS significantly improved depressive-like behavior in the (PSD+DMS) group compared to the PSD group. Glial cell activation and protein expression of inflammatory cytokines IL-1 β and TNF-α were increased in the frontal lobe of the stroke group. In the PSD group, further increase in glial cell activation and protein expression of IL-1 β and TNF-α was observed. However, in the (PSD + DMS) group, glial cell activation was reduced, and protein expression of IL-1 β and TNF-α was decreased. Conclusion: DMS treatment effectively improves depressive-like behavior in PSD rats. Inhibition of glial cell activation and expression of inflammatory cytokines in the frontal cortex may be potential mechanisms underlying its antidepressant effects.
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