Effect of Dilong composite agentia on major depressive disorder in mice
MU Yilan1#, HAN Li1#, JIANG Pengcheng1, WEI Siwen3, LUO Huaiqing2
1. The First Clinical College, Changsha Medical College, Changsha 410219, China; 2. School of Medicine, Hunan Normal University, Changsha 410013, China; 3. School of Medicine, Jishou University, Jishou 416000, China
Abstract:Objective To explore the effects of Dilong Composite Agentia (DCA) on mice with major depressive disorder (MDD). Methods The classical method-chronic unpredictable mild stress (CUMS) was used to construct MDD model. In the experiment, mice were evenly divided into control group, MDD group, MDD+ Paroxetine group and MDD + DCA group. We used the following techniques to indicate the results: sugar water preference experiments, tail suspension experiments, and forced swimming experiments for behavioral testing; HE staining to examine the pathological alterations in the hippocampal CA1 neurons of the mice; Immunohistochemical staining techniques to examine the expression of NF-κB in hippocampus. Using WB to detect the BDNF expression in hippocampal tissue and Elisa to detect the expression of TNF - α, IL-1β, and IL-6 in mouse brain tissue. Results The body weight of mice in the MDD+DCA group was apparently higher than that in the MDD group. The glucose preference rate of mice in the MDD+DCA group was significantly higher than that in the MDD group. The results of forced swimming and tail suspension experiments all showed that the stationary time of mice in the MDD+DCA group was significantly shorter than that in the MDD group. HE staining and immunohistochemical staining demonstrated that DCA significantly mitigated the pathological alterations in CA1 neurons of MDD mice induced by chronic unpredictable mild stress, along with a decrease in the expression of NF-κB. The expression of brain-derived neurotrophic factor (BDNF) protein of MDD+DCA group mice were obviously higher than that in the MDD group. The levels of TNF - α, IL-1 β, and IL-6 in the brain tissue of mice in the MDD+DCA group were apparently lower than in the MDD group. Conclusion Therefore, we conclude that DCA promotes neural repair and significantly improves depression behaviors through such mechanisms, which we propose with experimental evidence, that DCA increases BDNF expression in the hippocampal tissue and further reduces inflammation in the brain tissue of mice with depression.