RESUMO
Depression is one of the most common psychiatric conditions, characterized by significant and persistent depressed mood and diminished interest, and often coexists with various comorbidities. The underlying mechanism of depression remain elusive, evidenced by the lack of an appreciate therapy. Recent abundant clinical trials and animal studies support the new notion that the gut microbiota has emerged as a novel actor in the pathophysiology of depression, which partakes in bidirectional communication between the gut and the brain through the neuroendocrine, nervous, and immune signaling pathways, collectively known as the microbiota-gut-brain (MGB) axis. Alterations in the gut microbiota can trigger the changes in neurotransmitters, neuroinflammation, and behaviors. With the transition of human microbiome research from studying associations to investigating mechanistic causality, the MGB axis has emerged as a novel therapeutic target in depression and its comorbidities. These novel insights have fueled idea that targeting on the gut microbiota may open new windows for efficient treatment of depression and its comorbidities. Probiotics, live beneficial microorganisms, can be used to modulate gut dysbiosis into a new eubiosis and modify the occurrence and development of depression and its comorbidities. In present review, we summarize recent findings regarding the MGB axis in depression and discuss the potential therapeutic effects of probiotics on depression and its comorbidities.
Assuntos
Microbioma Gastrointestinal , Transtornos Mentais , Probióticos , Animais , Humanos , Encéfalo , Depressão/terapia , Disbiose/terapia , Microbioma Gastrointestinal/fisiologia , Probióticos/uso terapêuticoRESUMO
Introduction: Atherosclerosis (AS) is a chronic inflammatory disease characterized by lipid metabolism disorder and vascular endothelial damage. Albiflorin (AF) has been certified to be effective in the therapy of certain inflammatory diseases, while the therapeutic effect and mechanism of AF on AS have not been fully elucidated. Material and Methods. Model cells for AS were created by inducing oxidized low-density lipoprotein (Ox-LDL) in human umbilical vein endothelial cells (HUVECs). After processing with AF and interleukin-1 receptor-associated kinase 1- (IRAK1-) overexpressed plasmid, cell viability was assessed by CCK-8; cholesterol efflux was tested using liquid scintillation counter; IL-6 and TNF-α levels were determined with ELISA kits; ROS and apoptosis were confirmed using Flow cytometry. Besides, IRAK1-TAK1 pathway and apoptosis- and mitochondrial fusion-related proteins were monitored with western blotting analysis. Results: Our results verified that AF could not only dramatically accelerate viability and cholesterol efflux but also attenuate inflammation, ROS production, and apoptosis in Ox-LDL-induced HUVECs. Meanwhile, AF could prominently prevent the activation of IRAK1-TAK1 pathway, downregulate apoptosis-related proteins, and upregulate mitochondrial fusion-related proteins in Ox-LDL-induced HUVECs. Moreover, we testified that IRAK1 overexpression memorably could reverse suppression of AF on inflammation, apoptosis, and IRAK1-TAK1 pathway and enhancement of AF on viability, cholesterol efflux, and mitochondrial fusion in Ox-LDL-induced HUVECs. Conclusions: By blocking the IRAK1/TAK1 pathway, AF can significantly slow the course of AS, suggesting that it could be a viable therapeutic option for AS.
Assuntos
Aterosclerose , Quinases Associadas a Receptores de Interleucina-1 , Apoptose , Aterosclerose/metabolismo , Hidrocarbonetos Aromáticos com Pontes , Colesterol/metabolismo , Células Endoteliais da Veia Umbilical Humana/metabolismo , Humanos , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Quinases Associadas a Receptores de Interleucina-1/metabolismo , Lipoproteínas LDL/metabolismo , Espécies Reativas de Oxigênio/metabolismoRESUMO
A boy, aged 17 years, was admitted again due to abdominal pain, diarrhea, and eosinophilia for 3 years, which worsened for 3 days. Three years ago, the boy suffered from abdominal pain and diarrhea after eating yogurt; color Doppler ultrasound showed a large amount of peritoneal effusion, and routine blood test, bone marrow cell morphology, and ascites histological examination showed a large number of eosinophils. Three days ago, he was admitted again due to abdominal pain and diarrhea. The gastrointestinal endoscopy showed eosinophil infiltration in the angle of stomach. The boy was diagnosed with eosinophilic gastrointestinal disease (eosinophilic gastroenteritis). He was improved after the treatment with glucocorticoids and dietary avoidance, and no recurrence was observed during the one-year follow-up. It is concluded that for children who attend the hospital due to gastrointestinal symptoms such as abdominal pain and diarrhea, if there is an increase in peripheral blood eosinophils, it is necessary to consider the possibility of eosinophilic gastrointestinal disease, and eosinophil infiltration and abnormal eosinophil count in gastrointestinal tissue based on endoscopic biopsy may be the key to diagnosis.