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Neuropsychiatric disorders have been one of the worldwide health problems contributing to profound social and economic consequences. It is reported that consumption of an excessive high-fat diet (HFD) in middle age could induce cognitive and emotional dysfunctions, whereas the mechanisms of the effects of long-term HFD intake on brain disorders have not been fully investigated. We propose a hypothesis that prolonged HFD intake throughout adulthood could lead to neurobehavioral deterioration via gut-brain axis. In this study, the adult C57BL/6J mice consuming long-term HFD (24 weeks) exhibited more anxiety-like, depression-like, and disruptive social behaviors and poorer performance in learning and memory than control mice fed with a normal diet (ND). In addition, the homeostasis of gut microbiota was impaired by long-term HFD consumption. Changes in some flora, such as Prevotellaceae_NK3B31_group and Ruminococcus, within the gut communities, were correlated to neurobehavioral alterations. Furthermore, the gut permeability was increased after prolonged HFD intake due to the decreased thickness of the mucus layer and reduced expression of tight junction proteins in the colon. The mRNA levels of genes related to synaptic-plasticity, neuronal development, microglia maturation, and activation in the hippocampus and prefrontal cortex of HFD-fed mice were lower than those in mice fed with ND. Interestingly, the transcripts of genes related to tight junction proteins, ZO-1 and Occludin involved in blood-brain-barrier (BBB), were decreased in both hippocampus and prefrontal cortex after long-term HFD consumption. Those results indicated that chronic consumption of HFD in mice resulted in gut microbiota dysbiosis, which induced decreased expression of mucus and tight junction proteins in the colon, in turn leading to local and systemic inflammation. Those changes could further contribute to the impairment of brain functions and neurobehavioral alterations, including mood, sociability, learning and memory. In short, long-term HFD intake throughout adulthood could induce behavioral phenotypes related to neuropsychiatric disorders via gut-brain axis. The observations of this study provide potential intervention strategies to reduce the risk of HFD via targeting the gut or manipulating gut microbiota. [ABSTRACT FROM AUTHOR]

Gut microbiota is the key controller of healthy aging. Hypertension and osteoarthritis (OA) are two frequently co-existing age-related pathologies in older adults. Both are associated with gut microbiota dysbiosis. Hereby, we explore gut microbiome alteration in the Deoxycorticosterone acetate (DOCA)-induced hypertensive rat model. Captopril, an anti-hypertensive medicine, was chosen to attenuate joint damage. Knee joints were harvested for radiological and histological examination; meanwhile, fecal samples were collected for 16S rRNA and shotgun sequencing. The 16S rRNA data was annotated using Qiime 2 v2019.10, while metagenomic data was functionally profiled with HUMAnN 2.0 database. Differential abundance analyses were adopted to identify the significant bacterial genera and pathways from the gut microbiota. DOCA-induced hypertension induced p16INK4a+ senescent cells (SnCs) accumulation not only in the aorta and kidney (p < 0.05) but also knee joint, which contributed to articular cartilage degradation and subchondral bone disturbance. Captopril removed the p16INK4a + SnCs from different organs, partially lowered blood pressure, and mitigated cartilage damage. Meanwhile, these alterations were found to associate with the reduction of Escherichia-Shigella levels in the gut microbiome. As such, gut microbiota dysbiosis might emerge as a metabolic link in chondrocyte senescence induced by DOCA-triggered hypertension. The underlying molecular mechanism warrants further investigation. [ABSTRACT FROM AUTHOR]

Dietary intake of fermented soymilk is associated with hypotensive effects, but the mechanisms involved have not been fully elucidated. We investigated the anti-hypertensive effects of soymilk fermented by L. rhamnosus AC1 on DOCA-salt hypertension from the point of view of oxidative stress, inflammatory response and alteration of the gut microbiome. The antioxidant assays in vitro indicated the ethanol extract (EE) of L. rhamnosus AC1 fermented soymilk showed better antioxidative effects than the water extract (WE). Those extracts displayed a hypotensive effect using a tail-cuff approach to measuring blood pressure and improved nitric oxide (NO), angiotensin II (Ang II), tumor necrosis factor-α (TNF-α) and interleukin factor-6 (IL-6) on DOCA-salt hypertensive rats. Furthermore, cardiac and renal fibrosis were attenuated by those extracts. The gut microbiota analysis revealed that they significantly reduced the abundance of phylum Proteobacteria, its family Enterobacteriaceae and genus Escherichia-Shigella. Moreover, metabolomic profiling revealed several potential gut microbiota-related metabolites which appeared to involve in the development and recovery of hypertension. In conclusion, fermented soymilk is a promising nutritional intervention strategy to improve hypertension via reducing inflammation and reverting dysbiotic microbiota. [ABSTRACT FROM AUTHOR]

Among cardiovascular diseases (CVDs), a major cause of morbidity and mortality worldwide, coronary heart disease and stroke are the most well-known and extensively studied. The onset and progression of CVD is associated with multiple risk factors, among which, gut microbiota has received much attention in the past two decades. Gut microbiota, the microbial community colonizing in the gut, plays a prominent role in human health. In particular, gut dysbiosis is directly related to many acute or chronic dysfunctions of the cardiovascular system (CVS) in the host. Earlier studies have demonstrated that the pathogenesis of CVD is strongly linked to intestinal microbiota imbalance and inflammatory responses. Probiotics and prebiotics conferring various health benefits on the host are emerging as promising therapeutic interventions for many diseases. These two types of food supplements have the potential to alleviate the risks of CVD through improving the levels of several cardiovascular markers, such as total and low-density lipoprotein (LDL) cholesterol, high sensitivity C-reactive protein (hs-CRP), and certain cytokines involved in the inflammatory response. In this review, we focus mainly on the preventive effects of probiotics and prebiotics on CVD via rebalancing the structural and functional changes in gut microbiota and maintaining immune homeostasis. [ABSTRACT FROM AUTHOR]