Depression is a complex and prevalent mental illness. Cherry leaf is a traditional Chinese herbal medicine, which has confirmed to exert a certain antidepressant effect, but its potential neural regulation mechanism is not clear. This paper aims to investigate the improved action of cherry leaf decoction (CLD) on chronic unpredictable mild stress (CUMS) rats and its potential neural regulation mechanism by verifying the role and function of NMDAR regulatory target α2δ-1 in depression due to CUMS. Male SD rats were subjected to random stressors persisting for 5 weeks to establish the CUMS depression rat model. CLD could effectively alleviate depression-like behaviors of CUMS rats in behavioral tests including sucrose preference test, forced swimming test, tail suspension test and open field test. After the administration of the CLD, the expression of corticotropic-releasing hormone (CRH) in the hypothalamus was inhibited. Moreover, the levels of CRH, adrenal cortical hormone (ACTH) and corticosterone (CORT) in serum also decreased significantly. CUMS upregulated the expressions of α2δ-1, N-methyl- d -aspartate receptor 1 (NR1), NR2A and NR2B, and enhanced the binding ability to of α2δ-1 and NR1, which were reversed by CLD. The results demonstrated that CLD could ameliorate depression-like behaviors due to CUMS, which was related to the fact that CLD down-regulated α2δ-1 level and interfered with α2δ-1 binding to NR1, thereby reducing NMDAR expression and ultimately inhibiting HPA axis activity.
Scope Depression is the leading cause of disability around the world; however, most antidepressants have drug tolerance and serious side effects. In this study, it is explored whether partially hydrolyzed guar gum (PHGG) is a safe food that exhibits protection in a mouse model of depression. Methods and Results PHGG is orally administered to mice with depression induced by chronic unpredictable mild stress (CUMS) in two animal experiments (prevention trial and intervention trial) to characterize the potentially protective effect of PHGG. The results in the prevention trial show that PHGG significantly inhibits the loss of body weight, and prevents CUMS-induced depressive-like behavior in mice. The beneficial effects may be associated with PHGG modulating the gut microbiota structure and then increasing the levels of short-chain fatty acids in mice feces and the levels of 5-hydroxytryptamine and dopamine in serum, striatum, and hippocampus. Besides, PHGG in the intervention trial is less effective than that in the prevention trial, but it may have a synergistic effect on improving depression with fluoxetine. Conclusions This study suggests that moderate daily intake of PHGG can contribute to relieving depressive-like behavior.