Screening of the Antidepressant-Like Effect of the Traditional Chinese Medicinal Formula Si-Ni-San and Their Possible Mechanism of Action in Mice.

Screening of the antidepressant-like effect of the traditional Chinese medicinal formula Si-Ni-San and their possible mechanism of action in mice.

Pharmacognosy Res. 2013 1; 5(1): 36-42
Yi LT, Li J, Liu BB, Li CF

The traditional Chinese medicine formula Si-Ni-San has well therapeutic applications in improvement of mental diseases including depression. However, the neuropharmacological and neuroendocrine mechanisms of the formula on antidepressant-like action have not been reported.Herein, we explored the antidepressant-like effect and its mechanism of Si-Ni-San.Acute effect of Si-Ni-San on the immobility time was assessed in the mouse forced swim test (FST) and tail suspension test (TST). Moreover, we investigated the neurochemical, neuroendocrine, and neurotrophin systems involved in the antidepressant-like effect of this formula.Si-Ni-San significantly decreased the immobility time after acute treatment in the mouse TST (1300 mg/kg) but not in the FST compared with the control group. In addition, pretreatment of mice with PCPA or AMPT prevented the anti-immobility effect of Si-Ni-San (1300 mg/kg) in the TST. Moreover, acute Si-Ni-San (1300 mg/kg) decreased serum corticosterone levels, elevated serotonin (5-HT), norepinephrine (NE), and dopamine (DA) levels without affecting brain-derived neurotrophic factor (BDNF) levels in the whole brain exposed to TST.The acute antidepressant-like action of Si-Ni-San is mediated by the monoaminergic and neuroendocrine systems although underlying mechanism still remains to be further elucidated, and this formula should be further investigated as an alternative therapeutic approach for the treatment of depression. HubMed – depression


[Roles of cytokines in stress-induced depression.]

Sheng Li Xue Bao. 2013 Apr 25; 65(2): 229-236
Peng YL, Wang WY, Jiang CL, Wang YX

Depression is a very common mental health problem in our modern society. Stress is involved in the provocation of depression. The pathogenesis of depressive disorder is still not well known. The development of neuroendocrine immunology opens a new sight for clarification of mechanism underlying stress-induced depression. Chronic stress activates peripheral and central immune systems accompanied with the release of inflammatory mediators, including cytokines. Activated immune system mediates the process of depression through the interaction with neuron system and neuroendocrine system, including regulating the monoamine neurotransmitter system in synthesis, metabolism and reuptake, inducing the overactivation of hypothalamus-pituitary-adrenal (HPA) axis and its negative feedback regulation, and reducing neurogenesis. This present paper reviews the cytokines mechanisms underlying stress-induced depression. HubMed – depression



Retina. 2013 Apr 17;
Wolf A, Rüping J, Neubauer AS, Mayer W, Ulbig M, Haritoglou C, Holz FG, Eter N, Kampik A

PURPOSE:: To describe morphologic alterations of pigment epithelial detachments (PEDs) associated with neovascular age-related macular degeneration during anti-vascular endothelial growth factor upload therapy with ranibizumab. METHODS:: Prospective, single-arm interventional study. Primary outcome was the reduction of height of PED during monthly treatment using ranibizumab. Secondary outcomes were factors influencing the regression of PED. Inclusion criteria were presence of PED associated with naive neovascular age-related macular degeneration, visual acuity of >20/200, and height of PED >150 ?m on optical coherence tomography. All eyes (n = 54) received 3 injections of ranibizumab in monthly intervals (“upload therapy”). Last review examination was performed 14 weeks after the initial treatment. RESULTS:: The mean PED height decreased from 515 ?m (SD, 268.3) to 294 ?m (SD, 201.9) at Week 14 with the highest degree of regression after the first treatment. A complete resolution of PED was noted in 8 eyes (15%). Using conventional regression model, none of the factors investigated, including height of PED, presence of intraretinal or subretinal fluid, intraretinal cysts, macular volume, retinal thickness, presence of foveal depression, presence of hemorrhage, and visual acuity, had a significant impact on the morphologic response. Using a modified binary logistic regression model (“bootstrapping”), presence of foveal depression (P > 0.033), and retinal thickness (P > 0.004) showed statistical significance. CONCLUSION:: This study on the responses and potential predictive factors associated with vascularized PED during the uploading phase of intravitreal ranibizumab shows a complete resolution of the PED in 15% of the cases. HubMed – depression


Synthesis and evaluation of N-substituted nipecotic acid derivatives with an unsymmetrical bis-aromatic residue attached to a vinyl ether spacer as potential GABA uptake inhibitors.

Bioorg Med Chem. 2013 Apr 2;
Quandt G, Höfner G, Wanner KT

?-Amino butyric acid (GABA) is the major inhibitory neurotransmitter in the mammalian central nervous system (CNS). A malfunction of the GABAergic neurotransmission is connected to several neuronal disorders like epilepsy, Alzheimer’s disease, neuropathic pain, and depression. One possibility to enhance GABA levels in the synaptic cleft is to inhibit mGAT1, one of the four known plasma membrane bound GABA transporters, which is considered the most important GABA transporter subtype, being in charge of the removal of GABA from the synaptic cleft after a neuronal impulse. Lipophilic derivatives of nipecotic acid like Tiagabine (Gabitril®), an approved drug used in add-on therapy of epilepsy, are known to inhibit uptake of mGAT1 with high subtype selectivity and affinity. We synthesized new N-substituted nipecotic acid derivatives with a vinyl ether spacer and an unsymmetrical bis-aromatic residue, which carries fluorine substituents at various positions of the aromatic ring-system. The new compounds were characterized with respect to their potency and subtype selectivity as mGAT1 inhibitors. HubMed – depression