Background:Evidence from both clinical and experimental research indicates that the immune-brain interaction plays a pivotal role in the pathophysiology of depression. A multi-protein complex of the innate immune system, the NLRP3 inflammasome regulates cleavage and secretion of proinflammatory cytokine interleukin-1β. The inflammasome detects various pathogen-associated molecule patterns and damage-associated molecule patterns, which then leads to a series of immune-inflammatory reactions.Methods:To explore the role of inflammasome activation in the underlying biological mechanisms of depression, we established a mouse model of depression with unpredictable chronic mild stress.Results:Mice subjected to chronic mild stress for 4 weeks had significantly higher serum corticosterone levels, serum interleukin-1β levels, and hippocampal active interleukin-1β protein levels. They also displayed depressive-like symptoms, including decreased sucrose preference and increased immobility time. Moreover, the hippocampi of chronic mild stress-exposed mice had significantly higher activity of caspase-1, which accompanied by higher protein levels of NLRP3 and the apoptotic speck-containing protein with a card. Pretreatment with the NLRP3 inflammasome inhibitor VX-765 decreased serum and hippocampal levels of interleukin-1β protein and significantly moderated the depressive-like behaviors induced by chronic mild stress.Conclusions:These data suggest the NLRP3 inflammasome mediates stress-induced depression via immune activation. Future procedures targeting the NLRP3 inflammasome may have promising effects in the prevention and treatment of depression.

These data suggest for the first time that the NLRP3 inflammasome is involved in lipopolysaccharide-induced mice depressive-like behaviors. The NLRP3 inflammasome may be a central mediator between immune activation and depression, which raises the possibility that it may be a more specific target for the depression treatments in the near future.

BackgroundPrenatal depression can negatively affect the physical and mental health of both mother and fetus. The aim of this study was to determine the effectiveness of yoga as an intervention in the management of prenatal depression.MethodsA systematic review and meta-analysis of randomized controlled trials (RCTs) was conducted by searching PubMed, Embase, the Cochrane Library and PsycINFO from all retrieved articles describing such trials up to July 2014.ResultsSix RCTs were identified in the systematic search. The sample consisted of 375 pregnant women, most of whom were between 20 and 40 years of age. The diagnoses of depression were determined by their scores on Structured Clinical Interview for DSM-IV and the Center for Epidemiological Studies Depression Scale. When compared with comparison groups (e.g., standard prenatal care, standard antenatal exercises, social support, etc.), the level of depression statistically significantly reduced in yoga groups (standardized mean difference [SMD], −0.59; 95% confidence interval [CI], −0.94 to −0.25; p = 0.0007). One subgroup analysis revealed that both the levels of depressive symptoms in prenatally depressed women (SMD, −0.46; CI, −0.90 to −0.03; p = 0.04) and non-depressed women (SMD, −0.87; CI, −1.22 to −0.52; p < 0.00001) were statistically significantly lower in yoga group than that in control group. There were two kinds of yoga: the physical-exercise-based yoga and integrated yoga, which, besides physical exercises, included pranayama, meditation or deep relaxation. Therefore, the other subgroup analysis was conducted to estimate effects of the two kinds of yoga on prenatal depression. The results showed that the level of depression was significantly decreased in the integrated yoga group (SMD, −0.79; CI, −1.07 to −0.51; p < 0.00001) but not significantly reduced in physical-exercise-based yoga group (SMD, −0.41; CI, −1.01 to −0.18; p = 0.17).ConclusionsPrenatal yoga intervention in pregnant women may be effective in partly reducing depressive symptoms.Electronic supplementary materialThe online version of this article (doi:10.1186/s12888-015-0393-1) contains supplementary material, which is available to authorized users.

Emerging evidence suggests that neuroinflammation and oxidative stress may be major contributors to major depressive disorder (MDD). Patients or animal models of depression show significant increase of proinflammatory cytokine interleukin-1β (IL-1β) and oxidative stress biomarkers in the periphery or central nervous system (CNS). Recent studies show that hydrogen selectively reduces cytotoxic oxygen radicals, and hydrogen-rich saline potentially suppresses the production of several proinflammatory mediators. Since current depression medications are accompanied by a wide spectrum of side effects, novel preventative or therapeutic measures with fewer side effects might have a promising future. We investigated the effects of drinking hydrogen-rich water on the depressive-like behavior in mice and its underlying mechanisms. Our study show that hydrogen-rich water treatment prevents chronic unpredictable mild stress (CUMS) induced depressive-like behavior. CUMS induced elevation in IL-1β protein levels in the hippocampus, and the cortex was significantly attenuated after 4 weeks of feeding the mice hydrogen-rich water. Over-expression of caspase-1 (the IL-1β converting enzyme) and excessive reactive oxygen species (ROS) production in the hippocampus and prefrontal cortex (PFC) was successfully suppressed by hydrogen-rich water treatment. Our data suggest that the beneficial effects of hydrogen-rich water on depressive-like behavior may be mediated by suppression of the inflammasome activation resulting in attenuated protein IL-1β and ROS production.

The study suggested for the first time that nongenomic pathway was involved in GCs' rapid inhibition on allergic asthma, and raised the possibility of new therapeutic strategies for allergic diseases including asthma.

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