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BACKGROUND: The association between Life's essential 8 (LE 8), depression, and mortality still unexplored. METHODS: Data of 23,247 participants aged ≥20 years old were extracted from the National Health and Nutrition Examination Survey (NHANES) 2005-2018 in this retrospective cohort study. Depression symptoms were determined by the 9-item Patient Health Questionnaire (PHQ-9) and antidepressant use. Cardiovascular health was assessed using LE 8. Potential covariates were selected using weighted univariate Cox regression models. The associations of LE 8, depression symptoms, with mortality were explored via univariate and multivariate Cox proportional hazards models, and restricted cubic spline. And the relationships were further investigated with stratified by LE 8 scores. The results were presented as hazard ratios (HRs) and 95 % confidence intervals (CIs). RESULTS: Of the total 23,247 adults, 3208 (15.95 %) suffered from depression symptoms. After 99.75 months of mean follow-up time, 2400 individuals were died. Of these, 781 deaths were from cardiovascular disease (CVD). Depression symptoms were associated with higher odds of all-cause mortality (HR = 1.24, 95%CI: 1.06-1.45) and CVD mortality (HR = 1.36, 95%CI: 1.04-1.77). LE 8 score < 80 was marginal significance associated with all-cause mortality (HR = 1.14, 95%CI: 0.99-1.32). LE 8 had moderating effects on the associations of depression symptoms with all-cause (HR = 1.39, 95%CI: 1.16-1.67, P trend <0.05) and CVD mortality (HR = 1.63, 95%CI: 1.09-2.46, P trend <0.05). CONCLUSION: Higher LE 8 scores may moderate the association of depression symptoms with all-cause and CVD mortality. Adherence to healthier lifestyle behaviors may improve the prognosis of depression.
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The prevalence of depression continues to rise, and it has a high death and disability rate. Life's Essential 8 (LE8) is an updated measurement of cardiovascular health (CVH), and a higher score of LE8 represents healthier CVH. Our study aimed to investigate the association between the LE8 and depression among adults. This cross-sectional study used data from the National Health and Nutrition Examination Survey. CVH was measured by using LE8 according to American Heart Association definitions. Depression was assessed by the 9-item Patient Health Questionnaire (PHQ-9). Weighted univariable and multivariable logistic analyses were performed to investigate the association of LE8 with depression. Subgroup analyses were also conducted in different groups based on age, gender, race, body mass index (BMI), smoking, arthritis, cardiovascular disease, and chronic kidney disease. A total of 22,149 participants were included in the database, with a mean LE8 score of 71.27. The prevalence of depression was 7.32%. The mean scores of LE8 in health behaviors and health factors were 73.28 and 69.26, respectively. After adjustment of potential confounders, a higher LE8 score was associated with lower odds of depression (odds ratio = 0.27, 95% confidence interval: 0.20-0.37). A similar association was observed in the subgroup analyses. Higher overall LE8 scores and higher scores for each component (diet, physical activity, nicotine exposure, sleep duration, BMI, blood lipids, blood glucose, and blood pressure) were associated with lower odds of depression. LE8 score might be a useful tool for both cardiologists and psychiatrists in screening for and monitoring physical and mental health. Primary care physicians also could better tailor care and interventions to address both physical and mental health needs.
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Trametes robiniophila (Huaier) is available to refrain lung cancer (LC) cell progression, but its impact and mechanism on angiogenesis of LC are not proved. The study was to explore the potential mechanism of Huaier repressing angiogenesis and tumor growth in LC via strengthening let-7d-5p and targeting NAP1L1. Let-7d-5p and NAP1L1 expression was detected in LC tissues and cells (A549). Pretreatment of A549 cells was with Huaier. Transfection of changed let-7d-5p and NAP1L1 was to A549 cells to uncover their roles in LC cell progression with angiogenesis. Evaluation of the impact of let-7d-5p on angiogenesis in LC was in vitro in a mouse xenograft model. Identification of the targeting of let-7d-5p with NAP1L1 was clarified. The results clarified reduced let-7d-5p but elevated NAP1L1 were manifested in LC. Huaier restrained angiogenesis and tumor growth of LC in vivo and in vitro; Augmented let-7d-5p or declined NAP1L1 motivated the therapy of Huaier on LC; Let-7d-5p negatively modulated NAP1L1; Elevated NAP1L1 reversed the influence of enhancive let-7d-5p. These results strongly suggest that Huaier represses angiogenesis and tumor growth in LC via strengthening let-7d-5p and targeting NAP1L1. Huaier/let-7d-5p/NAP1L1 axis is supposed to be a promising target for the treatment of angiogenesis and tumor growth in LC via elevated let-7d-5p and targeted NAP1L1.
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Mezclas Complejas/farmacología , Neoplasias Pulmonares , MicroARNs/genética , Neovascularización Patológica/metabolismo , Proteína 1 de Ensamblaje de Nucleosomas/genética , Células A549 , Animales , Apoptosis/efectos de los fármacos , Femenino , Humanos , Pulmón/patología , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/patología , Ratones , Ratones Desnudos , TrametesRESUMEN
Chronic exposure to stressful environment is a key risk factor contributing to the development of depression. However, the mechanisms involved in this process are still unclear. Brain-derived neurotropic factor (BDNF) has long been investigated for its positive role in regulation of mood, although the role of its precursor, proBDNF, in regulation of mood is not known. In this study, using an unpredictable chronic mild stress (UCMS) paradigm we found that the protein levels of proBDNF were increased in the neocortex and hippocampus of stressed mice and this UCMS-induced upregulation of proBDNF was abolished by chronic administration of fluoxetine. We then established a rat model of UCMS and found that the expression of proBDNF/p75NTR/sortilin was upregulated, whereas the expression of mature BDNF and TrkB was downregulated in both neocortex and hippocampus of chronically stressed rats. Finally, we found that the injection of anti-proBDNF antibody via intracerebroventricular (i.c.v.) and intraperitoneal (i.p.) approaches into the UCMS rats significantly reversed the stress-induced depression-like behavior and restored the exploratory activity and spine growth. Although intramuscular injection of AAV-proBDNF did not exacerbate the UCMS-elicited rat mood-related behavioral or pathological abnormalities, i.c.v. injection of AAV-proBDNF increased the depression-like behavior in naive rats. Our findings suggest that proBDNF plays a role in the development of chronic stress-induced mood disturbances in rodents. Central (i.c.v.) or peripheral (i.p.) inhibition of proBDNF by injecting specific anti-proBDNF antibodies may provide a novel therapeutic approach for the treatment of stress-related mood disorders.
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Factor Neurotrófico Derivado del Encéfalo/metabolismo , Trastorno Depresivo/etiología , Transducción de Señal/fisiología , Estrés Psicológico/complicaciones , Animales , Anticuerpos/farmacología , Antidepresivos de Segunda Generación/farmacología , Antidepresivos de Segunda Generación/uso terapéutico , Encéfalo/efectos de los fármacos , Encéfalo/metabolismo , Factor Neurotrófico Derivado del Encéfalo/genética , Factor Neurotrófico Derivado del Encéfalo/inmunología , Enfermedad Crónica , Espinas Dendríticas/metabolismo , Espinas Dendríticas/ultraestructura , Trastorno Depresivo/tratamiento farmacológico , Modelos Animales de Enfermedad , Conducta Exploratoria/efectos de los fármacos , Fluoxetina/farmacología , Preferencias Alimentarias/efectos de los fármacos , Regulación de la Expresión Génica/efectos de los fármacos , Masculino , Ratones , Ratones Endogámicos C57BL , Precursores de Proteínas/biosíntesis , Precursores de Proteínas/metabolismo , Ratas , Ratas Wistar , Transducción de Señal/efectos de los fármacos , Estrés Psicológico/patología , Natación/psicologíaRESUMEN
The dysfunction of endothelial progenitor cells (EPCs) was found to be associated with vascular complications in diabetes mellitus (DM) patients. Previous studies found that regular exercise could improve the function of EPCs in DM patients, but the underling mechanism was unclear. Irisin, a newly identified myokine, was induced by exercise and has been demonstrated to mediate some of the positive effects of exercise. In this study, we hypothesize that irisin may have direct effects on EPC function in DM mice. These data showed for the first time that irisin increased the number of EPCs in peripheral blood of DM mice and improved the function of EPCs derived from DM mice bone marrow. The mechanism for the effect of irisin is related to the PI3K/Akt/eNOS pathway. Furthermore, irisin was demonstrated to improve endothelial repair in DM mice that received EPC transplants after carotid artery injury. The results of this study indicate a novel effect of irisin in regulating the number and function of EPCs via the PI3K/Akt/eNOS pathway, suggesting a potential for the administration of exogenous irisin as a succedaneum to improve EPC function in diabetic patients who fail to achieve such improvements through regular exercise.