Yang Xueping, Miao Junxiao, Huang Yinglin, Li Lili, Zhuang Gengsen
Department of Psychology, The People's Hospital of Liaoning Province, The people's hospital of China Medical University, Shenyang, Liaoning, China.
Department of Psychiatry, Sheng Jing Hospital of China Medical University, Shenyang, Liaoning, China.
Front Psychiatry. 2024 Jul 29;15:1425681. doi: 10.3389/fpsyt.2024.1425681. eCollection 2024.
Previous studies in different populations have shown that vitamin D supplementation may reduce depression levels. In adolescents, vitamin D deficiency has been identified as a factor contributing to the onset of depression. This study aimed to establish a model of adolescent depression in mice by using the scientific unpredictable chronic mild stress (UCMS) model and to preliminarily evaluate the effect of vitamin D on the occurrence and development of depression and whether it is related to the protein expression of the BDNF pathway.
The UCMS method was used to establish a model of adolescent depression in 4-week-old C57BL/6 male mice, randomly divided into five groups: Control group, Stress group, Stress+ low-dose group, Stress+ medium-dose group, Stress+ high-dose group. At the same time as chronic stress, the administration groups were given intramuscular injections of different doses of vitamin D. After 8 weeks, behavioral tests, including the forced swimming test (FST) and open field test (OFT), were performed on each group of mice, along with recording of indicators, blood vitamin D level detection, and brain tissue western blot analysis.
The results showed a significant difference in vitamin D levels among mice in different groups after 8 weeks (P=0.012). The results of behavioral testing showed a significant difference in the static time of forced swimming among the groups (P<0.001). Compared with the UCMS group, the static time of mice with vitamin D injection was significantly reduced (P<0.001). The total number of times mice entered the central area, the total distance of movement, and the time spent in the central area significantly increased after vitamin D injection compared with the UCMS-only group (all P<0.001). There was no significant difference in the expression of BDNF in the brain tissues of experimental mice (P>0.05).
In conclusion, in the mouse adolescent depression model, appropriate vitamin D supplementation can reduce the occurrence of stress-induced depression. Furthermore, vitamin D deficiency may also serve as a potential risk factor for depression.
先前在不同人群中的研究表明，补充维生素D可能会降低抑郁水平。在青少年中，维生素D缺乏已被确定为导致抑郁症发作的一个因素。本研究旨在通过使用科学的不可预测慢性轻度应激（UCMS）模型建立小鼠青少年抑郁症模型，并初步评估维生素D对抑郁症发生发展的影响以及它是否与BDNF通路的蛋白表达有关。
采用UCMS方法在4周龄的C57BL/6雄性小鼠中建立青少年抑郁症模型，随机分为五组：对照组、应激组、应激+低剂量组、应激+中剂量组、应激+高剂量组。在进行慢性应激的同时，给药组肌肉注射不同剂量的维生素D。8周后，对每组小鼠进行行为测试，包括强迫游泳试验（FST）和旷场试验（OFT），同时记录指标、检测血液维生素D水平以及进行脑组织蛋白质免疫印迹分析。
结果显示，8周后不同组小鼠的维生素D水平存在显著差异（P = 0.012）。行为测试结果显示，各组强迫游泳的静止时间存在显著差异（P < 0.001）。与UCMS组相比，注射维生素D的小鼠静止时间显著缩短（P < 0.001）。与仅进行UCMS的组相比，注射维生素D后小鼠进入中央区域的总次数、总移动距离以及在中央区域花费的时间均显著增加（均P < 0.001）。实验小鼠脑组织中BDNF的表达无显著差异（P > 0.05）。
总之,在小鼠青少年抑郁症模型中，适当补充维生素D可减少应激诱导的抑郁症的发生。此外，维生素D缺乏也可能是抑郁症的一个潜在危险因素。
