Microbial bionic nano-aromatic drugs for prevention of depression induced by chronic stress.

Depression is a mood disorder mainly clinically characterized by significant and persistent low spirits. Chronic stress is the leading cause of depression. However, traditional medicine has severe side effects in treating depression, ineffective treatment, and easy recurrence. Therefore, it is of great significance to prevent depression in the environment of chronic stress. In this study, aromatherapy was used for the prevention of depression. To solve the defects of intense volatility and inconvenience in using essential oils, we designed bionic nano-aromatic drugs and adhered them to the wallpaper. Inspired by the moldy wallpaper, we successively prepared the morphology-bionic nano-aromatic drugs, the function-bionic nano-aromatic drugs, and the bionic plus nano-aromatic drugs by referring to the morphology of microorganisms and substances in bacterial biofilms. Bionic nano-aromatic drugs remarkably promoted their adhesion on wallpaper. Molecular dynamics simulation explored its molecular mechanism. The essential oils, which were slowly released from the bionic nano-aromatic drugs, showed excellent biosecurity and depression prevention. These sustainedly released essential oils could significantly increase monoamine neurotransmitters in the brain under a chronic stress environment and had excellent neuroprotection. Besides, the bionic nano-aromatic drugs with simple preparation process and low cost had excellent application potential.

[Impacts of eye acupuncture on neurological deficit and Barthel index in patients of infarction hemiplegia].

OBJECTIVE: To observe the impacts of eye acupuncture on neurological deficit and Barthel index in the patients of infarction hemiplegia and explore its function mechanism. METHODS: Ninety-six patients of infarction hemiplegia were randomized into an observation group and a control group, 48 cases in each one. In the control group, the routine western medicines such as thrombolysis and antiplatelet aggregation were used. In the observation group, on the basis of the treatment as the control group, eye acupuncture was added at Shangjiao and Xiajiao areas bilaterally, once a day, 5 times a week. Separately, before treatment and after 2 weeks' treatment the score changes of the modified Edinburgh Scandinavia stroke scale (MESSS) and the activity of daily life scale (ADL, Barthel index, BI) were observed and the efficacy was compared between the two groups. The plasma endothelin was determined and compared before and after treatment in the two groups. RESULTS: After treatment, the effective rate was 93.8% (45/48) in the observation group and was 79.2% (38/48) in the control group. The effective rate in the observation group was higher apparently than that in the control group (P<0.05). The scores of neurological deficit were (13.29±1.45) and (18.24±1.33) in the observation group and control group respectively after treatment, which all lower apparently than (28.44±1.45) and (28.14±1.89) before treatment (both P<0.05). Additionally, the difference was significant between the two groups after treatment (P<0.05). The scores of Barthel index were (82.33±1.56) and (63.34±2.14) in the observation group and control group respectively, which all higher apparently than (38.53±1.54) and (38.14±2.56) before treatment (both P<0.05), and the difference was significant between the two groups after treatment (P<0.05). The levels of plasma endothelin were (54.55±11.48)ng/L and (62.44±9.88)ng/L in the observation group and the control group after treatment respectively, which were all lower apparently than (78.24±9.25)ng/L and (78.14±10.78)ng/L before treatment (both P<0.05). Additionally, the difference was significant between the two groups after treatment (P<0.05). CONCLUSIONS: Eye acupuncture effectively improves the neurological deficit and Brathel index in the patients of infarction hemiplegia and comprehensively improves the efficacy. The effect mechanism is possibly relevant with reducing plasma endothelin.

The Functional Study of a Chinese Herbal Compounded Antidepressant Medicine--Jie Yu Chu Fan Capsule on Chronic Unpredictable Mild Stress Mouse Model.

Jie Yu Chu Fan capsule (JYCF) is a new compounded Chinese herbal medicine for the treatment of depression. The present study was designed to explore the antidepressant effects and the possible mechanisms of JYCF by using chronic unpredictable mild stress (CUMS) mouse model and comparing results to that of fluoxetine. Behavioral tests including an open field test, sucrose preference test and forced swim test were performed to evaluate the antidepressant effects of JYCF. The concentrations of monoamine neurotransmitters and metabolic products including norepinephrine (NE), 5-hydroxytryptamine (5-HT), dopamine (DA), 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) in the cerebral cortex and hippocampus of mice were determined by means of high performance liquid chromatography with electrochemical detection (HPLC-EC). The results show that a successful mouse CUMS model was established through 5 weeks of continuous unpredictable stimulation, as indicated by the significant decrease in sucrose preference and locomotor activity and increase in immobility time in the forced swim test. Chronic treatment of JYCF (1.25, 2.5 and 5 g/kg) and fluoxetine (20 mg/kg) significantly reversed the CUMS-induced behavioral abnormalities. JYCF (1.25, 2.5 and 5 g/kg) significantly increased NE in CUMS mouse prefrontal cortex (P < 0.01, P < 0.01, P < 0.05 respectively) and 5-HT in hippocampus (P < 0.05). In summary, our findings suggest that JYCF exerts comparable antidepressant-like effects to that of fluoxetine in CUMS mice. Besides, the antidepressant-like effect of JYCF is mediated by the increase of monoaminergic transmitters including 5-HT and NE.

Emodin prevents hypoxic-ischemic neuronal injury: Involvement of the activin A pathway.

Emodin, an extract of dried rhizomes and the root of the Rhizoma Polygoni Cuspidati, can protect neurons from hypoxic-ischemic brain damage. This study aimed to verify the underlying mechanism. After PC12 cells had differentiated into neuron-like cells under the induction of mouse nerve growth factor, cells were subjected to oxygen-glucose deprivation and treated with emodin. Results showed that the viability of neuron-like cells cultured under an ischemia-hypoxia environment decreased, while the expression of activin A and caspase-3 in cells increased. Emodin raised the survival rate of oxygen-glucose deprived neuron-like cells, increased activin A expression, and decreased caspase-3 expression. Experimental findings indicate that emodin can inhibit neuronal apoptosis and alleviate the injury of nerve cells after oxygen-glucose deprivation through the activin A pathway.