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1.
Food Funct ; 10(9): 6062-6073, 2019 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-31486445

RESUMO

Depression is a mental disorder that brings severe burdens to patients and their families. Neuroinflammation and neurotrophins are involved in depression. Lotus plumule is a nutritional food with medicinal values. In the present study, we tried to clarify the anti-depressive effect and molecular mechanism of lotus plumule. Network pharmacological analysis, behavior tests, qRT-PCR and western blotting were used. We found 7 potential active components and 91 targets from the TCMSP database. KEGG analysis suggested that lotus plumule significantly affected nitrogen metabolism, calcium signaling, and inflammatory mediator regulation signaling pathways. Consistent with those effects, total alkaloids of lotus plumule (TLA) and active alkaloids differently suppressed the nitric oxide (NO) production and pro-inflammatory mediators. TLA and higenamine significantly ameliorated LPS-induced depression-like behavior, increased BDNF levels, suppressed microglia activation, and inhibited the expression of ER stress-related proteins. Meanwhile, TLA and higenamine activated microglia autophagy by increasing the beclin-1 and LC3B-II expression. Additionally, in the presence of autophagy inhibitor 3-MA, TLA and higenamine did not reduce the LPS-induced NO production or pro-inflammatory mediators. Collectively, TLA and higenamine attenuated LPS-induced depression-like behavior by regulating BDNF-mediated ER stress and autophagy. Therefore, drinking tea of lotus plumule may provide a potential strategy for preventing depression.


Assuntos
Alcaloides/administração & dosagem , Depressão/tratamento farmacológico , Lotus/química , Extratos Vegetais/administração & dosagem , Animais , Proteína Beclina-1/genética , Proteína Beclina-1/metabolismo , Comportamento Animal/efeitos dos fármacos , Fator Neurotrófico Derivado do Encéfalo/genética , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Depressão/induzido quimicamente , Depressão/metabolismo , Depressão/psicologia , Redes Reguladoras de Genes/efeitos dos fármacos , Humanos , Lipopolissacarídeos/efeitos adversos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Proteínas Associadas aos Microtúbulos/genética , Proteínas Associadas aos Microtúbulos/metabolismo , Sementes/química
2.
Int Immunopharmacol ; 75: 105788, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31377587

RESUMO

Depression has become a common mental illness, and studies have shown that neuroinflammation is associated with depression. Ketamine is a rapid antidepressant. In order to obtain better antidepressant effects, it is necessary to explore the efficacy of combination therapy with ketamine and other antidepressants. DHA is an unsaturated fatty acid with excellent application prospects due to its safety and antidepressant effects. This study was designed to investigate the effect of ketamine combined with DHA on lipopolysaccharide-induced depression-like behavior. In behavioral experiments, lipopolysaccharide prolongs the immobility time of the forced swimming and tail suspension tests in rats and reduces the sucrose preference. The combination of ketamine and DHA can reverse these changes and work better than the single application. Nissl staining showed that ketamine combined with DHA can reverse the nerve damage caused by lipopolysaccharide. Cell morphology observation the combination of ketamine and DHA group was more complete than that of LPS group. The combination of ketamine and DHA significantly decreased the levels of IL-1, IL-6 and TNF-ɑin hippocampus and PC12 cells and increased the content of BDNF. Immunofluorescence results showed that ketamine combined with DHA can effectively inhibit PP65 nuclear translocation. Western blot results showed that ketamine combined with DHA can effectively inhibit the expression of NF-KB in hippocampus and PC12 cells, and increase the expression of P-CREB and BDNF. In summary, the combination of ketamine with DHA may be a more effective treatment for depression caused by inflammation and is mediated by inhibition of the inflammatory pathway.


Assuntos
Antidepressivos/uso terapêutico , Depressão/tratamento farmacológico , Ácidos Docosa-Hexaenoicos/uso terapêutico , Ketamina/uso terapêutico , Animais , Antidepressivos/farmacologia , Comportamento Animal/efeitos dos fármacos , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo , Citocinas/metabolismo , Depressão/induzido quimicamente , Ácidos Docosa-Hexaenoicos/farmacologia , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Ketamina/farmacologia , Lipopolissacarídeos , Masculino , NF-kappa B/metabolismo , Células PC12 , Ratos , Ratos Wistar
3.
Pharmacol Biochem Behav ; 184: 172742, 2019 09.
Artigo em Inglês | MEDLINE | ID: mdl-31348944

RESUMO

Ketamine has become increasingly popular in adolescent drug abusers worldwide. Meanwhile, alcohol is usually used by ketamine users. However, little work has been conducted to examine the chronic combined effects of ketamine and ethanol on adolescent brain. Here we probed into the effects of chronic administration of ketamine at recreational doses alone or combined with ethanol on behaviors and neuron damage in an adolescent rat model. 28-day old rats were treated with either 20 or 30 mg/kg ketamine plus or not plus 10% ethanol daily for 21 days. Depressive like behaviors, anxiety like behavior and memory impairment were tested using open field test, forced swimming test, elevated plus maze and Morris water maze. Apoptosis in prefrontal cortex (PFC) and hippocampus (HIP) were determined by the TdT-mediated dUTP Nick-End Labeling (TUNEL) and protein and mRNA levels of caspase-3, Bax and Bcl-2. Results show that co-application of ketamine and ethanol significantly increased immobility time in the forced swimming test, up-regulated TUNEL positive cells and both protein and mRNA expressions of caspase-3 and Bax, compared with the control group and ketamine and ethanol use alone groups in the PFC, but not in the HIP. Our study suggests that chronic co-administration of ketamine and ethanol results in depressive-like behavior and the caspase-dependent apoptosis in the PFC of adolescent rats' brains.


Assuntos
Anestésicos Dissociativos/farmacologia , Apoptose/efeitos dos fármacos , Comportamento Animal/efeitos dos fármacos , Depressores do Sistema Nervoso Central/farmacologia , Etanol/farmacologia , Hipocampo/efeitos dos fármacos , Ketamina/farmacologia , Córtex Pré-Frontal/efeitos dos fármacos , Anestésicos Dissociativos/administração & dosagem , Animais , Ansiedade/induzido quimicamente , Caspase 3/genética , Caspase 3/metabolismo , Depressores do Sistema Nervoso Central/administração & dosagem , Depressão/induzido quimicamente , Etanol/administração & dosagem , Hipocampo/metabolismo , Ketamina/administração & dosagem , Masculino , Memória/efeitos dos fármacos , Córtex Pré-Frontal/metabolismo , Proteínas Proto-Oncogênicas c-bcl-2/genética , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Ratos , Ratos Sprague-Dawley , Proteína X Associada a bcl-2/genética , Proteína X Associada a bcl-2/metabolismo
4.
Acta Biochim Biophys Sin (Shanghai) ; 51(8): 834-844, 2019 Aug 05.
Artigo em Inglês | MEDLINE | ID: mdl-31314053

RESUMO

Our previous finding demonstrated that chronic corticosterone (CORT) may be involved in mediating the pathophysiology of premature aging in rats. Frequent jet lag increases the risk for many diseases, including obesity and type 2 diabetes, and is associated with the aging processes. However, the effect of jet lag on CORT-induced depression and its association with aging phenotypes remain unclear. In this study, the rats were exposed to both CORT and jet lag treatment, and the differences were analyzed and compared to rats with single CORT treatment. Our results showed that jet lag treatment aggravated CORT-induced depression-like behavior evidenced by sucrose intake test, forced swimming test, and open field test. Additionally, this treatment aggravated the shortening of telomeres, which possibly resulted in decreased telomerase activity, and downregulated the expression of telomere-binding factor 2 (TRF2) and telomerase reverse transcriptase compared to that in CORT rats, as revealed by quantitative real-time-polymerase chain reaction and western blot analysis, respectively. The shortening of telomeres may have been caused by increased oxidative stress, which was associated with the inhibition of sirtuin 3. Exposure to jet lag also aggravated the degeneration of mitochondrial functions, as shown by the decreases in the mRNA expression of COX1, ND1, and Tfam. Our findings provide physiological evidence that jet lag exposure may worsen stress-induced depression and age-related abnormalities.


Assuntos
Envelhecimento , Corticosterona/efeitos adversos , Depressão/etiologia , Síndrome do Jet Lag , Animais , Comportamento Animal , Corticosterona/administração & dosagem , Ciclo-Oxigenase 1/metabolismo , Depressão/induzido quimicamente , Fígado/efeitos dos fármacos , Fígado/patologia , Masculino , Proteínas de Membrana/metabolismo , NADH Desidrogenase/metabolismo , Estresse Oxidativo , Fenótipo , Ratos , Ratos Wistar , Sirtuína 3/antagonistas & inibidores , Proteínas Semelhantes à Proteína de Ligação a TATA-Box/metabolismo , Fatores de Transcrição/metabolismo
5.
Environ Int ; 131: 104927, 2019 10.
Artigo em Inglês | MEDLINE | ID: mdl-31326824

RESUMO

BACKGROUND: The association between air pollution exposure and emotional and behavioural problems in children is unclear. We aimed to assess prenatal and postnatal exposure to several air pollutants and child's depressive and anxiety symptoms, and aggressive symptoms in children of 7-11 years. METHODS: We analysed data of 13182 children from 8 European population-based birth cohorts. Concentrations of nitrogen dioxide (NO2), nitrogen oxides (NOx), particulate matter (PM) with diameters of ≤10 µm (PM10), ≤ 2.5 µm (PM2.5), and between 10 and 2.5 µm (PMcoarse), the absorbance of PM2.5 filters (PM2.5abs), and polycyclic aromatic hydrocarbons (PAHs) were estimated at residential addresses of each participant. Depressive and anxiety symptoms and aggressive symptoms were assessed at 7-11 years of age using parent reported tests. Children were classified in borderline/clinical range or clinical range using validated cut offs. Region specific models were adjusted for various socio-economic and lifestyle characteristics and then combined using random effect meta-analysis. Multiple imputation and inverse probability weighting methods were applied to correct for potential attrition bias. RESULTS: A total of 1896 (14.4%) children were classified as having depressive and anxiety symptoms in the borderline/clinical range, and 1778 (13.4%) as having aggressive symptoms in the borderline/clinical range. Overall, 1108 (8.4%) and 870 (6.6%) children were classified as having depressive and anxiety symptoms, and aggressive symptoms in the clinical range, respectively. Prenatal exposure to air pollution was not associated with depressive and anxiety symptoms in the borderline/clinical range (e.g. OR 1.02 [95%CI 0.95 to 1.10] per 10 µg/m3 higher NO2) nor with aggressive symptoms in the borderline/clinical range (e.g. OR 1.04 [95%CI 0.96 to 1.12] per 10 µg/m3 higher NO2). Similar results were observed for the symptoms in the clinical range, and for postnatal exposures to air pollution. CONCLUSIONS: Overall, our results suggest that prenatal and postnatal exposure to air pollution is not associated with depressive and anxiety symptoms or aggressive symptoms in children of 7 to 11 years old.


Assuntos
Poluentes Atmosféricos/análise , Ansiedade/epidemiologia , Depressão/epidemiologia , Exposição Ambiental/análise , Óxidos de Nitrogênio/análise , Material Particulado/análise , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Poluição do Ar/análise , Ansiedade/induzido quimicamente , Criança , Depressão/induzido quimicamente , Europa (Continente)/epidemiologia , Feminino , Humanos , Masculino , Dióxido de Nitrogênio/análise , Tamanho da Partícula , Gravidez , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Estudos Prospectivos
6.
Mediators Inflamm ; 2019: 7651383, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31281228

RESUMO

Many patients experience excellent physical recoveries after surgery; however, there are some of them who from suffer mood fluctuation, even depression. Postoperative depression may be resulted from cognitive dysfunction, pain, and a compromised immune system during the surgery. But there is a higher possibility that general anaesthesia may be responsible for the development of depression. Here, we employed one of the most used anaesthetics, propofol, in a mouse model to investigate whether this intravenous anaesthetic compound could cause depressive-like behavioural performance in mice. We found a single dose of propofol caused significant abnormal behavioural performance in tail suspension, forced swimming, and open field tests. We also examined the brain section of these mice and revealed that there was significant reduced expression of the CD11b protein, which demonstrated an inhibition of propofol on microglial function. We investigated the effect of propofol on synaptic protein, SYP, and found there was no notable influence on the protein expression. These above results suggested that propofol treatment might promote the depressive-like behaviours in mice via influencing the microglial cell function. Furthermore, we found the level of the IL-6 cytokine was significantly increased in the brain tissue, which might subsequently cause the activation of the transcriptional factor, STAT3. Our finding may provide a new perspective of further understanding the mechanism of anaesthetic drugs and deciphering the underlying mechanism of postoperative depression.


Assuntos
Depressão/induzido quimicamente , Microglia/efeitos dos fármacos , Microglia/fisiologia , Propofol/efeitos adversos , Anestesia Intravenosa , Animais , Ansiedade/induzido quimicamente , Ansiedade/metabolismo , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Antígeno CD11b/metabolismo , Depressão/metabolismo , Modelos Animais de Doenças , Ensaio de Imunoadsorção Enzimática , Interleucina-6/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Fator de Transcrição STAT3/metabolismo , Sinaptofisina/metabolismo
7.
Sci Total Environ ; 689: 1012-1022, 2019 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-31280147

RESUMO

The etiology of depression is not known, it is thought that endocrine-disrupting chemicals (EDCs) contribute to the disease. Results of our previous research have shown that nonylphenol (NP), a well-known EDC, has neurotoxic effects, however, whether NP can induce depressive behavior by affecting synaptic plasticity has not yet been clearly elucidated. The depressive behavior induced by subchronic exposure to NP and its effect on the neuronal synaptic plasticity in rats are dynamically observed. Thirty Sprague-Dawley rats were randomly divided into 3 groups: control group (C, corn oil), NP group (NP, 4 mg/kg), and depression model group (D, corticosterone 20 mg/kg). There were 8 rats in each group. The depressive behavior of rats was tested by sucrose preference test, open-field test, and forced swimming test once a month for 3 months. The serum levels of brain-derived neurotrophic factor (BDNF) and corticosterone were detected by ELISA assay, and cellular morphological changes were observed by hematoxylin-eosin (HE) staining. The number of nerve cells, the length of dendrites, and the density of dendritic spines were observed by Golgi staining, and the synaptic cleft width, the postsynaptic density (PSD) thickness, and the synaptic interface curvature were observed by transmission electron microscope. Compared with the control group, the consumption of sucrose solution decreased in the NP group at the 2nd and 3rd month compared to the 1st month (F = 9.887, P = 0.002). The number of central square entries, the central square duration, and the total distance of movement were all decreased, and the decreasing degrees at the 3rd month were greater than those at the 1st month (F = 21.191, P < 0.001; F = 9.836, P = 0.002). The time of immobility for the NP group at the 1st month was higher than that in the control group (F = 6.912, P = 0.002). The expression of BDNF in the NP-treated group was higher than the control, while the expression of corticosterone in the NP-treated group was lower than the control. In the NP group, the cytoplasm of nerve cells contracted and appeared disordered. The neuron arrangement was disordered, and the number of cells, the length of the apex, the length of the basal dendrites, and the dendritic spine density were all lower in the NP group than those in the control group. The PSD thickness, the synaptic cleft width, and synaptic interface curvatures were all decreased in the NP group when compared to the control group. Subchronic exposure to 4 mg/kg NP led to depressive behavior in rats, and the depressive behavior and alterations in synaptic plasticity were more obvious with longer exposure time.


Assuntos
Fator Neurotrófico Derivado do Encéfalo/sangue , Depressão/fisiopatologia , Disruptores Endócrinos/toxicidade , Glucocorticoides/sangue , Plasticidade Neuronal/efeitos dos fármacos , Fenóis/toxicidade , Animais , Depressão/induzido quimicamente , Córtex Pré-Frontal/efeitos dos fármacos , Córtex Pré-Frontal/fisiopatologia , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley
8.
Neurotox Res ; 36(2): 396-410, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31201731

RESUMO

The neurotoxicity of immunosuppressive agents and diabetes mellitus are known risk factors of neurological complications in kidney transplant recipients. The aim of the present study was to investigate the influence of tacrolimus on brain-derived neurotrophic factor (BDNF), the critical protein for maintenance of neuronal functions, in the hippocampus in a diabetic condition. A diabetic rat model was established by a single streptozotocin injection (60 mg/kg). Control and diabetic rats then received daily tacrolimus (1.5 mg/kg per day) injections for 6 weeks. BDNF expression in the hippocampus was examined in the dentate gyrus (DG) and CA3 region using immunohistochemistry. There was a significant decrease of BDNF expression in the DG and CA3 region in tacrolimus-treated and diabetic rats compared with that of the control group injected with vehicle only. However, there was no difference in BDNF expression between the two experimental groups. Tacrolimus treatment in diabetic rats further decreased the BDNF expression level in the DG and CA3 region. Interestingly, mossy fiber sprouting, demonstrated by prominent punctate immunolabeling of BDNF with synaptoporin, was observed in the diabetic group treated with tacrolimus, which localized at the stratum oriens of the CA3 region. These data suggest that tacrolimus treatment or a diabetic condition decreases BDNF expression in the hippocampus, and that tacrolimus treatment in the diabetic condition further injures the CA3 region of the hippocampus. In addition to BDNF expression, decreased locomotor activity and evident depressive behavior were observed in tacrolimus-treated diabetic rats. Moreover, there were significant decreases of the mRNA levels of γ-aminobutyric acid and serotonin receptors in the diabetic hippocampus with tacrolimus treatment. This finding suggests that tacrolimus treatment may cause further psychiatric and neurological complications for patients with diabetes, and should thus be used with caution.


Assuntos
Depressão/induzido quimicamente , Depressão/metabolismo , Diabetes Mellitus Experimental/metabolismo , Hipocampo/metabolismo , Imunossupressores/toxicidade , Tacrolimo/toxicidade , Animais , Fator Neurotrófico Derivado do Encéfalo , Depressão/patologia , Diabetes Mellitus Experimental/patologia , Hipocampo/efeitos dos fármacos , Hipocampo/patologia , Masculino , Ratos , Ratos Sprague-Dawley
9.
Artigo em Chinês | MEDLINE | ID: mdl-31177719

RESUMO

Objective: Clinical analysis of sequelae of 16 patients with trimethyltin chloride (TMT) poisoning after 2 years. Methods: Sixteen patients with TMT poisoning from a waste recycling company in Ganzhou City in August 2016 were enrolled. They were investigated by questionnaires and assessed by various scales after two years. 6 cases of severe poisoning were examined by head MRI. The scale includes Hamilton Anxiety Scale (HAMA) , Depression Scale (HAMD) , Simple Mental State Examination Scale (MMSE) , Activity of Daily Living (ADL) , International Cooperative Ataxia Rating Scale (ICARS) . Results: 16 cases of TMT poisoning still have headache, dizziness and other symptoms. Instability of walking in 4 patients with severe poisoning, and the brain MRI manifestations included obvious atrophy of temporal lobe, hippocampus, insula lobe, cerebellum and ventricle enlargement. Two patients were rated as severe mixed anxiety and depression, one as moderate mixed anxiety and depression, and one as mild anxiety. 3 cases were diagnosed as dementia and 1 case as mild cognitive impairment. Two cases were totally dependent on living ability. ICARS scores were 66 points and 63 points respectively. Two cases were mildly dependent on living ability. ICARS scores were 28 points and 6 points respectively. There were 2 cases of mild mixed anxiety and depression in mild and moderate poisoning patients, and 1 case of mild cognitive impairment in each patient. They could live independently. ICARS scores were 0. Conclusion: After 2 years of TMT poisoning, some patients still have general clinical symptoms such as dizziness, headache and so on. There are also mental and intellectual symptoms such as anxiety, depression and cognitive impairment. Some of patients with severe poisoning presented with dementia and cerebellar ataxia, and even lost independent living ability.


Assuntos
Atividades Cotidianas , Transtornos Cognitivos , Depressão , Compostos de Trimetilestanho , Transtornos Cognitivos/induzido quimicamente , Demência/induzido quimicamente , Depressão/induzido quimicamente , Progressão da Doença , Seguimentos , Humanos , Exposição Ocupacional , Óxidos , Reciclagem , Compostos de Trimetilestanho/envenenamento
10.
Mediators Inflamm ; 2019: 6212934, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31210750

RESUMO

Background: Systemic inflammation impairs cognitive performance, yet the brain networks mediating this process remain to be elucidated. The purpose of the current study was to use resting-state functional magnetic resonance imaging (fMRI) to explore changes in the functional connectivity in a lipopolysaccharide- (LPS-) induced systemic inflammation animal model. Materials and Methods: We used the regional homogeneity (ReHo) method to examine abnormal brain regions between the control and LPS groups and then considered them as seeds of functional connectivity analysis. Results: Compared with the control group, our study showed that (1) LPS impaired mood function, as reflected by a depression-like behavior in the forced swim test; (2) LPS induced significantly increased ReHo values in the anterior cingulate cortex (ACC) and caudate putamen (CPu); (3) the ACC seed showed increased functional connectivity with the retrosplenial cortex, superior colliculus, and inferior colliculus; and (4) the right CPu seed showed increased functional connectivity with the left CPu. Linear regression analysis showed a LPS-induced depression-like behavior which was associated with increased ReHo values in the ACC and right CPu. Moreover, the LPS-induced depression-like behavior was related to increased functional connectivity between the right CPu and left CPu. Conclusion: This is the first study to show that systemic inflammation impairs mood function that is associated with an altered resting-state functional network based on ReHo analysis, providing evidence of the abnormal regional brain spontaneous activity which might be involved in inflammation-related neurobehavioral abnormalities.


Assuntos
Afeto/efeitos dos fármacos , Depressão/metabolismo , Inflamação/fisiopatologia , Lipopolissacarídeos/toxicidade , Animais , Depressão/induzido quimicamente , Ensaio de Imunoadsorção Enzimática , Inflamação/metabolismo , Imagem por Ressonância Magnética , Masculino , Ratos , Ratos Sprague-Dawley
11.
Neuropharmacology ; 155: 150-161, 2019 09 01.
Artigo em Inglês | MEDLINE | ID: mdl-31145906

RESUMO

Lysophosphatidic acid (LPA) is a bioactive lipid mediator of inflammation that binds to its specific cell surface G protein coupled receptors (LPA1-6). It is reported that LPA induced cell apoptosis by targeting LPA1, while LPA1 blockade eliminated LPS-induced production of peritoneal neutrophil chemokines and cytokines. Previous studies have shown that Saikosaponin-d (SSd) mitigated depressive-like behaviors in rats exposed to chronic unpredictable mild stress (CUMS), as well as corticosterone-induced apoptosis in PC12 cells. The present study explored the role of SSd during modulating LPA1 mediated neuronal apoptosis in LPS-stimulated mice. The phenomenon that SSd alleviated LPS-induced depressive-like behaviors were observed by open field test (OPT), forced swim test (FST) and tail suspension test (TST). SSd inhibited the protein expression of LPA1 both in the CA1 and CA3 region of the hippocampus. Moreover, SSd significantly decreased the levels of RhoA, ROCK2, p-p38, p-ERK, p-p65, p-IκBα in LPS-stimulated mice as well as in LPA-stimulated SH-SY5Y cells. Additionally, SSd significantly decreased the expression of LPA1 and the degree of neuronal apoptosis in SH-SY5Y cells which were co-cultured with LPS-stimulated BV2 microglia. These results suggested that SSd improved LPS-induced depressive-like behaviors in mice and suppressed neuronal apoptosis by regulating LPA1/RhoA/ROCK2 signaling pathway.


Assuntos
Anti-Inflamatórios não Esteroides/metabolismo , Apoptose/fisiologia , Depressão/metabolismo , Neurônios/metabolismo , Ácido Oleanólico/análogos & derivados , Receptores de Ácidos Lisofosfatídicos/metabolismo , Saponinas/metabolismo , Animais , Anti-Inflamatórios não Esteroides/farmacologia , Anti-Inflamatórios não Esteroides/uso terapêutico , Apoptose/efeitos dos fármacos , Linhagem Celular Tumoral , Técnicas de Cocultura , Depressão/induzido quimicamente , Depressão/tratamento farmacológico , Relação Dose-Resposta a Droga , Humanos , Lisofosfolipídeos/metabolismo , Lisofosfolipídeos/toxicidade , Camundongos , Camundongos Endogâmicos ICR , Neurônios/efeitos dos fármacos , Ácido Oleanólico/metabolismo , Ácido Oleanólico/farmacologia , Ácido Oleanólico/uso terapêutico , Distribuição Aleatória , Saponinas/farmacologia , Saponinas/uso terapêutico
12.
Croat Med J ; 60(2): 71-77, 2019 Apr 30.
Artigo em Inglês | MEDLINE | ID: mdl-31044578

RESUMO

AIM: To test the hypothesis that valproic acid treatment positively affects brain-derived neurotrophic factor (BDNF) expression and DNA methylation in the hippocampus and brain cortex of rats simultaneously treated with aldosterone. METHODS: Male Sprague-Dawley rats (N=40) were treated for two weeks with valproic acid (100 mg/1 kg body weight/d) in drinking water and aldosterone (2 µg/100 g body weight/d) or placebo via subcutaneous osmotic minipumps. RESULTS: Treatment with valproic acid did not modify BDNF gene expression in the hippocampus but reduced BDNF mRNA levels in the brain cortex. Valproic acid treatment marginally enhanced global DNA methylation in the frontal cortex. BDNF expression negatively correlated with DNA methylation in the hippocampus of valproic acid-treated rats. An unexpected finding was that aldosterone treatment significantly decreased global DNA methylation in the hippocampus. CONCLUSION: The effect of valproic acid on BDNF expression in the brain may depend on the extent of pathological changes present at the time of treatment onset. The observed negative correlation between BDNF expression and DNA methylation in the hippocampus of valproic acid-treated rats encourages further studies.


Assuntos
Fator Neurotrófico Derivado do Encéfalo/metabolismo , Metilação de DNA/efeitos dos fármacos , Depressão/tratamento farmacológico , Hipocampo/efeitos dos fármacos , Ácido Valproico/farmacologia , Aldosterona , Animais , Encéfalo/metabolismo , Córtex Cerebral/metabolismo , Depressão/induzido quimicamente , Modelos Animais de Doenças , Hipocampo/metabolismo , Masculino , RNA Mensageiro/metabolismo , Ratos , Ratos Sprague-Dawley , Ácido Valproico/uso terapêutico
13.
Biomed Chromatogr ; 33(9): e4542, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30947404

RESUMO

A highly selective and efficient LC-MS/MS method was developed to determine the plasma concentration of magnolol, hesperidin, neohesperidin and geniposide following oral administration of Zhi-Zi-Hou-Po decoction in normal and depressed rats. Plasma samples were pretreated by protein precipitation with methanol. Chromatographic separation was performed on an XTerra® MS C18 column using a gradient elution with a mobile phase composed of acetonitrile-0.1% aqueous formic acid. The proposed method was validated to be specific, accurate and precise for the analytes determination in plasma samples. The calibration curves displayed good linearity over definite concentration ranges for the analytes. The intra- and inter-day precision of the proposed method at three different levels were all within <11.13% and the relative errors ranged from -8.46 to 8.93%. The recovery of the four compounds ranged from 82.72 to 89.08% and no apparent matrix effect was observed during sample analysis. After full validation, the established method was successfully applied for comparing the pharmacokinetics of four components between normal and depressed rats. The results showed that the AUC and Cmax of four analytes in depressed rats were significantly different from those in normal rats and might provide helpful information to guide the clinical use of Zhi-Zi-Hou-Po to treat depression.


Assuntos
Depressão , Medicamentos de Ervas Chinesas/farmacocinética , Iridoides/farmacocinética , Administração Oral , Animais , Compostos de Bifenilo/sangue , Compostos de Bifenilo/química , Compostos de Bifenilo/farmacocinética , Corticosterona/efeitos adversos , Depressão/induzido quimicamente , Depressão/metabolismo , Modelos Animais de Doenças , Medicamentos de Ervas Chinesas/administração & dosagem , Hesperidina/sangue , Hesperidina/farmacocinética , Iridoides/administração & dosagem , Iridoides/sangue , Iridoides/química , Lignanas/sangue , Lignanas/química , Lignanas/farmacocinética , Limite de Detecção , Modelos Lineares , Masculino , Ratos , Ratos Sprague-Dawley , Reprodutibilidade dos Testes
14.
Psychopharmacology (Berl) ; 236(9): 2667-2676, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30941469

RESUMO

RATIONALE: Illicit use of anabolic androgenic steroids (AAS) has grown into a serious public health concern throughout the Western World. AAS use is associated with adverse medical, psychological, and social consequences. Around 30% of AAS users develop a dependence syndrome with sustained use despite adverse side effects. AAS dependence is associated with a high frequency of intra- and interpersonal problems, and it is central to identify factors related to the development and maintenance of dependence. METHODS: The present study investigated the ability to recognize emotion from biological motion. The emotional biological motion task was administered to male AAS dependent users (AAS dependents; n = 45), AAS non-dependent users (AAS non-dependents; n = 38) and a comparison-group of non-using weightlifters (non-users; n = 69). RESULTS: Multivariate analysis of variance showed a general impairment in emotion recognition in AAS dependents, compared to the non-using weightlifters, whereas no significant impairment was observed in AAS non-dependents. Furthermore, AAS dependents showed impaired recognition of fearful stimuli compared to both AAS non-dependents and non-using weightlifters. The between-group effect remained significant after controlling for Intelligence Quotient (IQ), past 6 months of non-AAS drug use, antisocial personality problems, anxiety, and depression. CONCLUSION: AAS dependents show impaired emotion recognition from body movement, fear in particular, which could potentially contribute to higher frequency of interpersonal problems and antisocial behaviors in this population.


Assuntos
Anabolizantes/efeitos adversos , Androgênios/efeitos adversos , Emoções/efeitos dos fármacos , Movimento/efeitos dos fármacos , Transtornos Relacionados ao Uso de Substâncias/psicologia , Adulto , Anabolizantes/administração & dosagem , Androgênios/administração & dosagem , Transtornos de Ansiedade/induzido quimicamente , Transtornos de Ansiedade/psicologia , Estudos Transversais , Depressão/induzido quimicamente , Depressão/psicologia , Emoções/fisiologia , Humanos , Masculino , Movimento/fisiologia , Estimulação Luminosa/métodos , Treinamento de Resistência/métodos , Transtornos Relacionados ao Uso de Substâncias/diagnóstico , Congêneres da Testosterona/administração & dosagem , Congêneres da Testosterona/efeitos adversos , Adulto Jovem
15.
Artigo em Inglês | MEDLINE | ID: mdl-30991759

RESUMO

Previous studies have suggested an association between secondhand smoke (SHS) exposure and risk of depressive symptoms. However, it remains unclear whether there is a dose-response relationship. The effect estimates were pooled using fixed-effect or random-effect models based on homogeneity analysis. The dose-response meta-analysis was performed by linear and non-linear regression. Subgroup analyses were conducted to explore the possible sources of heterogeneity. Twenty-four studies were included in this meta-analysis. SHS exposure was significantly associated with increased odds of depressive symptoms (odds ratio (OR) = 1.32, 95% confidence interval (CI) 1.25-1.39). For SHS exposure expressed as an ordinal variable, the dose-response meta-analysis revealed a monotonically increasing relationship between SHS exposure and depressive symptoms. A similar dose-response relationship was observed for SHS exposure expressed as a continuous variable (OR = 1.57, 95% CI = 1.26-1.87). Our findings suggest that SHS exposure is associated with increasing odds of depressive symptoms in a dose-response manner.


Assuntos
Depressão/epidemiologia , Poluição por Fumaça de Tabaco/análise , Depressão/induzido quimicamente , Relação Dose-Resposta a Droga , Humanos , Prevalência , Fatores de Risco
16.
BMC Med ; 17(1): 78, 2019 04 15.
Artigo em Inglês | MEDLINE | ID: mdl-30982472

RESUMO

BACKGROUND: Ultra-processed food (UPF) consumption has increased over the last decades in Westernized countries. Our objective was to investigate for the first time the association between the proportion of UPF (%UPF) in the diet and incident depressive symptoms in the NutriNet-Santé cohort. METHODS: The sample included 20,380 women and 6350 men (aged 18-86 years) without depressive symptoms at the first Center for Epidemiologic Studies Depression Scale (CES-D) measurement, using validated cut-offs (CES-D score ≥ 17 for men and ≥ 23 for women). The proportion of UPF in the diet was computed for each subject using the NOVA classification applied to dietary intakes collected by repeated 24-h records (mean = 8; SD = 2.3). The association between UPF and depressive symptoms was evaluated using multivariable Cox proportional hazards models. RESULTS: Over a mean follow-up of 5.4 years, 2221 incident cases of depressive symptoms were identified. After accounting for a wide range of potential confounders, an increased risk of depressive symptoms was observed with an increased %UPF in the diet. In the main model adjusted for sociodemographic characteristics, body mass index, and lifestyle factors, the estimated hazard ratio for a 10% increase in UPF was 1.21 (95% confidence interval = 1.15-1.27). Considering %UPF in food groups, the association was significant only for beverages and sauces or added fats. CONCLUSION: Overall, UPF consumption was positively associated with the risk of incident depressive symptoms, suggesting that accounting for this non-nutritional aspect of the diet could be important for mental health promotion.


Assuntos
Depressão/induzido quimicamente , Dieta/psicologia , Fast Foods/efeitos adversos , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Estudos de Coortes , Depressão/patologia , Feminino , França , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Adulto Jovem
17.
Artigo em Inglês | MEDLINE | ID: mdl-31022424

RESUMO

The dysfunction of mitochondria plays important roles in the development of depression. Interestingly, increasing numbers of evidence show the therapeutic benefits of mitochondria transfer. Therefore, we hypothesized that injection of exogenous mitochondria would contribute to ameliorate depressive-like symptoms. In this study, the antidepressant-like effect of intravenous isolated mitochondria was evaluated on a lipopolysaccharide (LPS)- induced model of depression. The depressive-like behaviors were assessed using forced swim test (FST), tail suspension test (TST) and sucrose preference test. Besides, the neurogenesis, expression of brain-derived neurotrophic factor (BDNF), glial activation, neuroinflammation, oxidative stress and ATP production were determined in the hippocampus. The results showed that treatment of isolated mitochondria decreased the immobility time of mice in the FST and TST, and attenuated the decrease in sucrose preference test. Moreover, isolated mitochondria significantly reduced the activation of astrocyte and microglia as well as neuroinflammation (i.e. 1 L-1ß, TNF-α and COX-2), increased BDNF expression and neurogenesis, restored the dysfunction of ATP production and oxidative stress in inflammation- induced depression. Taken together, the data suggested for the first time that injection of isolated mitochondria ameliorated LPS- induced depressive-like behaviors. The new discovery for the present study provides that mitochondrial transplantation might act as a new therapeutic strategy for MDD.


Assuntos
Depressão/terapia , Lipopolissacarídeos/farmacologia , Mitocôndrias/transplante , Trifosfato de Adenosina/metabolismo , Animais , Western Blotting , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Depressão/induzido quimicamente , Modelos Animais de Doenças , Fator 9 de Crescimento de Fibroblastos/metabolismo , Imunofluorescência , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos ICR , Atividade Motora , Estresse Oxidativo , Reação em Cadeia da Polimerase em Tempo Real
18.
Psychiatry Res ; 276: 69-78, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-31029037

RESUMO

Recent studies have reported an association between air pollution exposure and depression, with inconsistent results. To address this controversy, we conducted a systematic review and meta-analysis of published observational studies that investigated outdoor air pollution and depression. Five electronic databases were searched, and fifteen articles were finally identified. Pooled odds risks were calculated separately based on pollutant type, exposure duration and outcome. Subgroup analyses were conducted based on design, population, important potential confounders, and pollutants levels. We found a significantly increased risk of depression with long-term exposure to PM2.5 and short-term exposure to PM10, NO2, SO2, CO. No evidence was found in the association between exposure to O3 and depression. Besides, exposure to high levels of pollutants indicates a higher risk of depression. Our results highlight the necessity of air pollution control for depression. However, further studies with standardized methods are still required to support the results due to the inconsistent results in stratified analyses and methodological limitations of the included studies.


Assuntos
Poluição do Ar/efeitos adversos , Depressão/induzido quimicamente , Depressão/psicologia , Exposição Ambiental/efeitos adversos , Estudos Observacionais como Assunto/métodos , Material Particulado/efeitos adversos , Bases de Dados Factuais , Depressão/epidemiologia , Humanos , Estudos Prospectivos
19.
Neuroscience ; 406: 126-139, 2019 05 15.
Artigo em Inglês | MEDLINE | ID: mdl-30825582

RESUMO

Ethanol ingestion by a mother during pregnancy entails adverse consequences for her offspring. In this study, adult female rats were given access to ethanol from 8 days prior to mating to post-parturition weaning, and the effects on her offspring were evaluated. We investigated changes in the cocaine- and amphetamine-regulated transcript peptide (CART), a neuropeptide involved in the central effects of ethanol in the frame of reward and stress processing circuits. CART-immunoreactivity was augmented in the cells of Edinger-Westphal (EW) nucleus and lateral hypothalamus (LH) and fibers in the LH and ventral tegmental area (VTA) in 25-day-old pups. On the other hand, a significant decrease was seen in the expression of the peptide in paraventricular nucleus (PVN), arcuate nucleus (ARC), hippocampus (CA1 and CA2) and locus coeruleus (LC). The offspring at 85 days showed increased anxiety in elevated plus maze and immobility in forced swim test suggestive of depression. These rats also failed to discriminate between novel versus familiar object in object recognition test indicating memory deficits. Their brains showed decreased CART-immunoreactivity in nucleus accumbens shell, lateral bed nucleus of stria terminalis, PVN, ARC, LH, hippocampus and LC as compared to age-matched control offspring. However, CART-immunoreactive profile in EW and fibers in VTA of 85-day-old offspring was similar to that in the control. Thus, regional imbalance in the CART system of the offspring of alcoholic dams seems correlated with the affective and emotional abnormalities and memory deficits.


Assuntos
Ansiedade/metabolismo , Encéfalo/metabolismo , Depressão/metabolismo , Etanol/efeitos adversos , Transtornos da Memória/metabolismo , Proteínas do Tecido Nervoso/biossíntese , Efeitos Tardios da Exposição Pré-Natal/metabolismo , Animais , Ansiedade/induzido quimicamente , Encéfalo/efeitos dos fármacos , Depressão/induzido quimicamente , Etanol/administração & dosagem , Feminino , Masculino , Transtornos da Memória/induzido quimicamente , Gravidez , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Ratos , Ratos Sprague-Dawley
20.
Neurosci Lett ; 701: 180-192, 2019 05 14.
Artigo em Inglês | MEDLINE | ID: mdl-30825591

RESUMO

Depression is a major health issue that causes severe societal economic and health burden. Aromatherapy, a practice that uses essential oils for preventive and therapeutic purposes, represents a promising therapeutic alternative for the alleviation of depressive symptoms. Lavender essential oil (LEO) has been the focus of clinical studies due to its positive effect on mood. An animal model of chronic administration of high dose corticosterone to induce depression- and anxiety-like behavior and reduced neurogenesis was used to explore the biological changes brought by aromatherapy. Twenty-four adult male Sprague Dawley rats were randomly assigned into four groups: Control, corticosterone (Cort) group with high dose of corticosterone, LEO group with daily exposure to LEO by inhalation, and LEO + Cort. At the end of the 14-day treatment period, behavioral tests were carried out. Serum samples were collected 2-3 days after the 14-day period treatment and before perfusion to carry out biochemical analyses to measure BDNF, corticosterone and oxytocin. After perfusion, brains were collected for immunohistochemical analysis to detect BrdU and DCX positive cells in the hippocampus and subventricular zone. Results showed that treatment with LEO ameliorated the depression-like behavior induced by the chronic administration of corticosterone as observed in the LEO + Cort group. Cort treatment reduced the number of BrdU positive cells in the hippocampus and the subventricular zone. Treatment with LEO prevented the corticosterone-induced reduction in the number of BrdU positive cells (LEO + Cort group) demonstrating the neurogenic effect of LEO under high corticosterone conditions. Chronic administration of high dose of corticosterone significantly reduced the dendritic complexity of immature neurons. On the contrary, treatment with LEO increased dendritic complexity of immature neurons under high corticosterone conditions (LEO + Cort group). The improved neurogenesis and dendritic complexity observed in the LEO + Cort group demonstrated a clear restorative effect of LEO under high corticosterone conditions. However, 2-3 days after the treatment, the levels of BDNF were upregulated in the LEO and LEO + Cort groups. Furthermore, the concentration of oxytocin in serum, 2-3 days after the treatment, showed to be upregulated in the LEO group alone. The present study has provided evidence of the biological effect of LEO on neuroplasticity and neurogenesis. Also, this study contributes to the understanding of the mechanism of action of LEO in an animal model where depression- and anxiety-like behavior and reduced neurogenesis were induced by high corticosterone administration.


Assuntos
Ansiedade/patologia , Ansiedade/psicologia , Comportamento Animal/efeitos dos fármacos , Dendritos/efeitos dos fármacos , Depressão/patologia , Depressão/psicologia , Lavandula/química , Óleos Voláteis/farmacologia , Óleos Vegetais/farmacologia , Animais , Ansiedade/induzido quimicamente , Corticosterona , Dendritos/patologia , Depressão/induzido quimicamente , Masculino , Neurogênese , Plasticidade Neuronal/efeitos dos fármacos , Ratos Sprague-Dawley
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