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。

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.